subject:(angiotensin II)

Tulane University

1. Cypress, Michael. Sodium-glucose co-transporter 2 mediates angiotensinogen augmentation in renal proximal tubular cells under high glucose conditions.

Degree: 2017, Tulane University

URL: https://digitallibrary.tulane.edu/islandora/object/tulane:76911

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Increased activity of the intrarenal renin-angiotensin system (RAS), in which proximal tubular angiotensinogen (AGT) is a key factor, has been implicated in the progression of… (more)

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Increased activity of the intrarenal renin-angiotensin system (RAS), in which proximal tubular angiotensinogen (AGT) is a key factor, has been implicated in the progression of diabetic nephropathy. AGT expression is upregulated in renal proximal tubular cells (PTC) by high glucose due to elevated reactive oxygen species (ROS) generation. Angiotensin II (Ang II) also promotes ROS generation. Glucose reabsorption in PTC occurs mainly through sodium-glucose co-transporter 2 (SGLT2). This study was performed to demonstrate that SGLT2 mediates AGT augmentation in PTC under hyperglycemic conditions. Furthermore, the enhancing effect of Ang II was investigated. Established mouse PTC were treated with 5 (normal), 15, or 25 mM D-glucose or D-mannitol (osmotic control). Pyruvate was used to investigate the role of glycolysis on AGT regulation. Glycolytic activity was quantified using a Seahorse metabolic analyzer. Tempol, an antioxidant, was used to determine the role of ROS. SGLT2 expression was silenced using shRNA. PTC were treated with high glucose and 10-10-10-7 M Ang II or an Ang II receptor blocker. AGT protein levels were increased by 15 (4.4 ± 0.2-fold over control) and 25 mM (4.6 ± 0.2-fold) glucose. AGT mRNA was also augmented (31.1 ± 3.5-fold) by 25 mM glucose, but not mannitol. AGT expression was stimulated by pyruvate (10.7 ± 1.0-fold over control), and exposure to 10, 15, or 25 mM glucose increased glycolytic activity (3.10 ± 0.28-fold, 2.74 ± 0.20-fold, and 2.75 ± 0.34-fold, respectively), suggesting that enhanced glycolysis stimulates AGT expression. ROS accumulation increased (3.03 ± 0.29-fold) in 25 mM glucose over control. Tempol attenuated glucose-induced AGT augmentation by 77%, suggesting that ROS generation contributes to AGT upregulation. SGLT2 knockdown prevented AGT augmentation in 15 mM glucose, indicating that SGLT2 plays a key role mediating AGT upregulation by high glucose. Ang II receptor blockade did not alter AGT levels, and Ang II did not enhance AGT expression in normal or high glucose. Similarly, SGLT2 expression was unchanged by glucose or Ang II. These results indicate that SGLT2 contributes to AGT upregulation in PTC by high glucose, which helps to explain the mechanisms causing intrarenal RAS activation and consequent diabetic nephropathy.

1

Michael W. Cypress

Advisors/Committee Members: (author), Sato, Ryosuke (Thesis advisor), School of Science & Engineering Cell and Molecular Biology (Degree granting institution).

Subjects/Keywords: Angiotensin II

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Cypress, M. (2017). Sodium-glucose co-transporter 2 mediates angiotensinogen augmentation in renal proximal tubular cells under high glucose conditions. (Thesis). Tulane University. Retrieved from https://digitallibrary.tulane.edu/islandora/object/tulane:76911

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Cypress, Michael. “Sodium-glucose co-transporter 2 mediates angiotensinogen augmentation in renal proximal tubular cells under high glucose conditions.” 2017. Thesis, Tulane University. Accessed March 03, 2021. https://digitallibrary.tulane.edu/islandora/object/tulane:76911.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Cypress, Michael. “Sodium-glucose co-transporter 2 mediates angiotensinogen augmentation in renal proximal tubular cells under high glucose conditions.” 2017. Web. 03 Mar 2021.

Vancouver:

Cypress M. Sodium-glucose co-transporter 2 mediates angiotensinogen augmentation in renal proximal tubular cells under high glucose conditions. [Internet] [Thesis]. Tulane University; 2017. [cited 2021 Mar 03]. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:76911.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Cypress M. Sodium-glucose co-transporter 2 mediates angiotensinogen augmentation in renal proximal tubular cells under high glucose conditions. [Thesis]. Tulane University; 2017. Available from: https://digitallibrary.tulane.edu/islandora/object/tulane:76911

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Edinburgh

2. Ashek, Ali. Altered renal function and the development of angiotensin II-dependent hypertension.

Degree: PhD, 2011, University of Edinburgh

URL: http://hdl.handle.net/1842/5568

► Inappropriate modulation of the renin angiotensin system (RAS) can lead to derangements of blood pressure homeostasis in humans. Cyp1a1-mRen2.F transgenic rats were used to define… (more)

▼ Inappropriate modulation of the renin angiotensin system (RAS) can lead to derangements of blood pressure homeostasis in humans. Cyp1a1-mRen2.F transgenic rats were used to define the renal mechanisms underlying the development of angiotensin II-dependent hypertension. These transgenic rats were previously generated by introducing the mouse Ren2 gene into the rat genome under the control of a Cyp1a1 inducible promoter. The aim of the current investigation was to establish the contribution of renal function to the development of hypertension in the Cyp1a1- mRen2.F transgenic rat. Expression of the mRen2 transgene was induced by daily gavage of indole 3 carbinol (I3C) at the dose of 100mg/kg. Blood pressure was measured in conscious rats after 1, 3 or 7 days of treatment. The control group received the vegetable oil carrier for 7 days. In addition blood pressure, renal haemodynamics and excretory function were measured under thiobutabarbital anaesthesia. Transgene induction caused a progressive increase in blood pressure in a time dependent manner. Neither glomerular filtration rate nor renal blood flow was affected. This indicates proper function of renal autoregulation during the experimental time course. Tubular sodium reabsorption was significantly increased after the first day of transgene induction and this effect was sustained for the duration of treatment. A pharmacological approach was used to localize the increased reabsorption to a specific region of the nephron and was found to reflect increased activity of the thiazide-sensitive cotransporter (NCC). Chronic administration of thiazide significantly blunted the hypertensive response to transgene induction. Similarly AT1 receptor blockade attenuated the hypertensive phenotype and prevented the transgene-induced stimulation of NCC activity. In contrast, mineralocorticoid receptor blockade did not prevent the development of either hypertension or increased NCC activity. The current study suggests that the development of angiotensin II-dependent hypertension is mediated by increased tubular sodium reabsorption. Increased activity of NCC is a key hypertensive mechanism in this model and results directly from the actions of angiotensin II at the AT1 receptor; indirect aldosterone pathways do not play a major role.

Subjects/Keywords: 616.1; hypertension; kidney; angiotensin; angiotensin II; NCC

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Ashek, A. (2011). Altered renal function and the development of angiotensin II-dependent hypertension. (Doctoral Dissertation). University of Edinburgh. Retrieved from http://hdl.handle.net/1842/5568

Chicago Manual of Style (16^th Edition):

Ashek, Ali. “Altered renal function and the development of angiotensin II-dependent hypertension.” 2011. Doctoral Dissertation, University of Edinburgh. Accessed March 03, 2021. http://hdl.handle.net/1842/5568.

MLA Handbook (7^th Edition):

Ashek, Ali. “Altered renal function and the development of angiotensin II-dependent hypertension.” 2011. Web. 03 Mar 2021.

Vancouver:

Ashek A. Altered renal function and the development of angiotensin II-dependent hypertension. [Internet] [Doctoral dissertation]. University of Edinburgh; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1842/5568.

Council of Science Editors:

Ashek A. Altered renal function and the development of angiotensin II-dependent hypertension. [Doctoral Dissertation]. University of Edinburgh; 2011. Available from: http://hdl.handle.net/1842/5568

3. 坂元, 紀陽. Adrenomedullin Does Not Contribute toward the Development of Abdominal Aortic Aneurysm in Mice : 腹部大動脈瘤形成におけるアドレノメデュリンの役割.

Degree: 博士(医学), 2014, University of Miyazaki / 宮崎大学

URL: http://hdl.handle.net/10458/4934

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以下に掲載:Health. 2014, 6, 10, p.1077-1084, doi: 10.4236/health.2014.610133###This work is licensed under the Creative Commons Attribution International License (CC BY).

Abdominal aortic aneurysm (AAA) develops based… (more)

Subjects/Keywords: Aneurysm; Angiotensin II; Aortic Rupture

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

坂元, �. (2014). Adrenomedullin Does Not Contribute toward the Development of Abdominal Aortic Aneurysm in Mice : 腹部大動脈瘤形成におけるアドレノメデュリンの役割. (Thesis). University of Miyazaki / 宮崎大学. Retrieved from http://hdl.handle.net/10458/4934

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

坂元, 紀陽. “Adrenomedullin Does Not Contribute toward the Development of Abdominal Aortic Aneurysm in Mice : 腹部大動脈瘤形成におけるアドレノメデュリンの役割.” 2014. Thesis, University of Miyazaki / 宮崎大学. Accessed March 03, 2021. http://hdl.handle.net/10458/4934.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

坂元, 紀陽. “Adrenomedullin Does Not Contribute toward the Development of Abdominal Aortic Aneurysm in Mice : 腹部大動脈瘤形成におけるアドレノメデュリンの役割.” 2014. Web. 03 Mar 2021.

Vancouver:

坂元 �. Adrenomedullin Does Not Contribute toward the Development of Abdominal Aortic Aneurysm in Mice : 腹部大動脈瘤形成におけるアドレノメデュリンの役割. [Internet] [Thesis]. University of Miyazaki / 宮崎大学; 2014. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10458/4934.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

坂元 �. Adrenomedullin Does Not Contribute toward the Development of Abdominal Aortic Aneurysm in Mice : 腹部大動脈瘤形成におけるアドレノメデュリンの役割. [Thesis]. University of Miyazaki / 宮崎大学; 2014. Available from: http://hdl.handle.net/10458/4934

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Oregon State University

4. Niibori, Yoshiko. Regulation of inositol phospholipid hydrolysis by extended treatment with angiotensin II in human aortic smooth muscle cells.

Degree: MS, Pharmacy, 2003, Oregon State University

URL: http://hdl.handle.net/1957/30353

► Long-term stimuli of many systems leads to decreased cellular responsiveness, or desensitization. We characterized the desensitization of angiotensin II (Ang 11)-mediated inositol phospholipid (IP) hydrolysis… (more)

Subjects/Keywords: Angiotensin II

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Niibori, Y. (2003). Regulation of inositol phospholipid hydrolysis by extended treatment with angiotensin II in human aortic smooth muscle cells. (Masters Thesis). Oregon State University. Retrieved from http://hdl.handle.net/1957/30353

Chicago Manual of Style (16^th Edition):

Niibori, Yoshiko. “Regulation of inositol phospholipid hydrolysis by extended treatment with angiotensin II in human aortic smooth muscle cells.” 2003. Masters Thesis, Oregon State University. Accessed March 03, 2021. http://hdl.handle.net/1957/30353.

MLA Handbook (7^th Edition):

Niibori, Yoshiko. “Regulation of inositol phospholipid hydrolysis by extended treatment with angiotensin II in human aortic smooth muscle cells.” 2003. Web. 03 Mar 2021.

Vancouver:

Niibori Y. Regulation of inositol phospholipid hydrolysis by extended treatment with angiotensin II in human aortic smooth muscle cells. [Internet] [Masters thesis]. Oregon State University; 2003. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1957/30353.

Council of Science Editors:

Niibori Y. Regulation of inositol phospholipid hydrolysis by extended treatment with angiotensin II in human aortic smooth muscle cells. [Masters Thesis]. Oregon State University; 2003. Available from: http://hdl.handle.net/1957/30353

University of Southern California

5. Nguyen, Mien Thi Xuan. Integrated regulation of transporters along the nephron to maintain electrolyte and fluid homeostatis.

Degree: PhD, Integrative Biology of Disease, 2013, University of Southern California

URL: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/294063/rec/3532

► The kidneys play an essential role in regulating blood pressure (BP) and maintaining fluid and electrolyte homeostasis. The balance is achieved by an integrative network… (more)

▼ The kidneys play an essential role in regulating blood pressure (BP) and maintaining fluid and electrolyte homeostasis. The balance is achieved by an integrative network of hormones and nerves that signal changes in Na⁺ and K⁺ transporters along the nephron under various stimuli, such as hypokalemia, elevated circulating plasma AngII concentration, and high BP. The regulation could be either acute or chronic via trafficking, covalent modification, or changes in total transporter abundance. Taking an integrative approach to generate transporter profiles along the nephron, this dissertation aimed to determine 1) the effects of K⁺-deficient diets with and without NaCl supplementation on Na⁺, K⁺, and H₂O transporters’ abundance; 2) how transporters are differentially regulated in AngII-dependent hypertension model: a balance between blood pressure vs. AngII; and 3) the renal responses at the early stage of AngII infusion without accompanying hypertension. Results: 1) Despite profound hypokalemia and renal K⁺ conservation with K⁺-deficient diets, most transporters’ abundance was not altered as previously reported in the literature; there was primarily a decrease in the sodium channel whose activity drives K⁺ secretion, but no change in the K⁺ transporter. We predict that changes in their distribution and activity are likely more important for conserving K⁺ than changes in total pool size, since they need to act quickly when an animal suddenly switches from a K⁺-deprived mode to a K⁺-replete mode. 2) In AngII-dependent hypertension, we reported a differential regulation of Na⁺ transporters along the nephron: distal stimulation counteracted by proximal inhibition to obtain a homeostatic balance. We postulate that starting from the cortical TALH through the medullary CD, AngII has an anti-natriuretic action on Na⁺ transporters to increase Na⁺ reabsorption in the distal region of the nephron, while pressure-natriuresis acts along the proximal nephron, starting from the PT through the medullary TALH, to reduce Na⁺ reabsorption. 3) At the early stage of AngII infusion, we demonstrated that Na⁺ transporters are activated in both the proximal tubule and distal nephron, creating a pre-hypertensive state, which likely increases Na⁺ reabsorption in these regions to contribute to the development of hypertension observed with longer infusion periods. Overall, these studies illustrate that a determination of changes in ion transporter along the entire nephron are necessary to ascertain how fluid and electrolyte homeostasis is maintained in the face of changes in intake or experimental hypertension. Advisors/Committee Members: McDonough, Alicia A. (Committee Chair), Peti-Peterdi, Janos (Committee Member), Chow, Robert H. (Committee Member), Okamoto, Curtis Toshio (Committee Member).

Subjects/Keywords: transporters; hypertension; angiotensin II; hypokalemia

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nguyen, M. T. X. (2013). Integrated regulation of transporters along the nephron to maintain electrolyte and fluid homeostatis. (Doctoral Dissertation). University of Southern California. Retrieved from http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/294063/rec/3532

Chicago Manual of Style (16^th Edition):

Nguyen, Mien Thi Xuan. “Integrated regulation of transporters along the nephron to maintain electrolyte and fluid homeostatis.” 2013. Doctoral Dissertation, University of Southern California. Accessed March 03, 2021. http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/294063/rec/3532.

MLA Handbook (7^th Edition):

Nguyen, Mien Thi Xuan. “Integrated regulation of transporters along the nephron to maintain electrolyte and fluid homeostatis.” 2013. Web. 03 Mar 2021.

Vancouver:

Nguyen MTX. Integrated regulation of transporters along the nephron to maintain electrolyte and fluid homeostatis. [Internet] [Doctoral dissertation]. University of Southern California; 2013. [cited 2021 Mar 03]. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/294063/rec/3532.

Council of Science Editors:

Nguyen MTX. Integrated regulation of transporters along the nephron to maintain electrolyte and fluid homeostatis. [Doctoral Dissertation]. University of Southern California; 2013. Available from: http://digitallibrary.usc.edu/cdm/compoundobject/collection/p15799coll3/id/294063/rec/3532

University of Manchester

6. Nguyen, Binh Yen. The Cardioprotective Role of Prolyl Carboxypeptidase (PRCP) in Cardiac Hypertrophic Remodelling.

Degree: 2020, University of Manchester

URL: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:323033

► With increasing prevalence and incidence rates over time, heart failure is well-recognised as a chronic disease with lifelong management, and is one of the top… (more)

Subjects/Keywords: Heart; Hypertrophy; Angiotensin II; Angiotensin 1-7; Prolyl Carboxypeptidase (PRCP)

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Nguyen, B. Y. (2020). The Cardioprotective Role of Prolyl Carboxypeptidase (PRCP) in Cardiac Hypertrophic Remodelling. (Doctoral Dissertation). University of Manchester. Retrieved from http://www.manchester.ac.uk/escholar/uk-ac-man-scw:323033

Chicago Manual of Style (16^th Edition):

Nguyen, Binh Yen. “The Cardioprotective Role of Prolyl Carboxypeptidase (PRCP) in Cardiac Hypertrophic Remodelling.” 2020. Doctoral Dissertation, University of Manchester. Accessed March 03, 2021. http://www.manchester.ac.uk/escholar/uk-ac-man-scw:323033.

MLA Handbook (7^th Edition):

Nguyen, Binh Yen. “The Cardioprotective Role of Prolyl Carboxypeptidase (PRCP) in Cardiac Hypertrophic Remodelling.” 2020. Web. 03 Mar 2021.

Vancouver:

Nguyen BY. The Cardioprotective Role of Prolyl Carboxypeptidase (PRCP) in Cardiac Hypertrophic Remodelling. [Internet] [Doctoral dissertation]. University of Manchester; 2020. [cited 2021 Mar 03]. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:323033.

Council of Science Editors:

Nguyen BY. The Cardioprotective Role of Prolyl Carboxypeptidase (PRCP) in Cardiac Hypertrophic Remodelling. [Doctoral Dissertation]. University of Manchester; 2020. Available from: http://www.manchester.ac.uk/escholar/uk-ac-man-scw:323033

NSYSU

7. Li, Ping-tao. Differential Roles of Angiotensin II Type 1 and Type 2 Receptors at Rostral Ventrolateral Medulla in a Mevinphos Intoxication Model of Brain Stem Death.

Degree: Master, Biological Sciences, 2009, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-123213

► The rostral ventrolateral medulla (RVLM) is the origin of a âlife-and-deathâ signal identifies from systemic arterial blood pressure spectrum that reflects failure of central cardiovascular… (more)

▼ The rostral ventrolateral medulla (RVLM) is the origin of a âlife-and-deathâ signal identifies from systemic arterial blood pressure spectrum that reflects failure of central cardiovascular regulation during brain stem death. It is also a target site where endogenous angiotensin II acts on angiotensin II type 1 receptors (AT1R) to increase blood pressure (BP); or on type 2 receptors (AT2R) to inhibit baroreceptor reflex (BRR) response. This study investigated the roles of AT1R and AT2R and their signaling pathways in RVLM for âlife-and-deathâ signal response during experimental brain stem death, using organophosphate mevinphos (Mev) as the experimental insult. In Sprague-Dawley rats, Mev (640 Î¼g/kg, i.v.) elicited an increase (pro-life phase) followed by a decrease (pro-death phase). Real-time PCR analysis revealed that whereas AT1R level underwent a 10% increase at pro-life phase, AT2R exhibited a significance increase of up to 40% at pro-death phase. Western blot analysis revealed that whereas AT1R level underwent a 20% increase at pro-life phase, AT2R exhibited a significant increase of up to 50% at pro-death phase. Pretreatment with microinjection of an AT1R antagonist losartan (2 nmol) into RVLM elicited abrupt death because of drastic hypotension through inhibiting NADPH oxidase and its downstream superoxide anion. Pretreatment with NADPH oxidase inhibitor DPI (1.5 nmol) inhibited NADPH oxidase avtiviting and superoxide anion production and decreased âlife-and-deathâ signal at pro-life phase; using superoxide anion inhibitor tempol (5 nmol) potentiated blood pressure and âlife-and-deathâ signal at pro-death phase. However, pretreatment with an AT2R antagonist PD123319 (2 nmol) potentiated the âlife-and-deathâ signal and antagonized hypotension during pro-death phase through inhibiting protein phosphotase 2A (PP2A) then activating extracellular signal-regulated kinase 1/2 (ERK1/2). Similar to AT2R antagonist PD123319, pretreatment with PP2A inhibitor okadaic acid (0.5 fmol) inhibit PP2A, leading to activation of ERK1/2, potentiate âlife-and-deathâ signal and antagonized hypotension during pro-death phase. These results suggest that AT1R in RVLM plays a âpro-lifeâ role through NADPH oxidase/superoxide anion during experimental brain stem death by maintaining BP and âlife-and-deathâ signal; AT2R plays a âpro-deathâ role through PP2A/ERK1/2 by inhibiting BP and âlife-and-deathâ signal, and superoxide may also plays a âpro-life and pro-deathâ role at pro-death phase. Advisors/Committee Members: Julie Y.H. Chan (chair), Alice Y.W. Chang (committee member), Samuel H.H. Chan (chair).

Subjects/Keywords: Angiotensin II; RVLM; Mev; brain stem death

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Li, P. (2009). Differential Roles of Angiotensin II Type 1 and Type 2 Receptors at Rostral Ventrolateral Medulla in a Mevinphos Intoxication Model of Brain Stem Death. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-123213

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Li, Ping-tao. “Differential Roles of Angiotensin II Type 1 and Type 2 Receptors at Rostral Ventrolateral Medulla in a Mevinphos Intoxication Model of Brain Stem Death.” 2009. Thesis, NSYSU. Accessed March 03, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-123213.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Li, Ping-tao. “Differential Roles of Angiotensin II Type 1 and Type 2 Receptors at Rostral Ventrolateral Medulla in a Mevinphos Intoxication Model of Brain Stem Death.” 2009. Web. 03 Mar 2021.

Vancouver:

Li P. Differential Roles of Angiotensin II Type 1 and Type 2 Receptors at Rostral Ventrolateral Medulla in a Mevinphos Intoxication Model of Brain Stem Death. [Internet] [Thesis]. NSYSU; 2009. [cited 2021 Mar 03]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-123213.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Li P. Differential Roles of Angiotensin II Type 1 and Type 2 Receptors at Rostral Ventrolateral Medulla in a Mevinphos Intoxication Model of Brain Stem Death. [Thesis]. NSYSU; 2009. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-0825109-123213

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Ruhr Universität Bochum

8. Schulte, Kathrin. NO/cGMP-vermittelte Signaltransduktion : Aufklärung der direkten und indirekten Interaktion mit kontraktilen Faktoren innerhalb der Gefäßregulation.

Degree: 2012, Ruhr Universität Bochum

URL: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-40692

► Wichtige Gegenspieler bei der Einstellung des Gefäßtonus stellen die relaxierende NO/cGMP-vermittelte Signaltransduktion und die kontraktilen Faktoren, Angiotensin II, der Hauptmetabolit des Renin-Angiotensin-Systems, und das aus… (more)

Subjects/Keywords: Cyclo-GMP; Angiotensin II; Noradrenalin; Gefäßtonus; Blutdruck

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APA (6^th Edition):

Schulte, K. (2012). NO/cGMP-vermittelte Signaltransduktion : Aufklärung der direkten und indirekten Interaktion mit kontraktilen Faktoren innerhalb der Gefäßregulation. (Thesis). Ruhr Universität Bochum. Retrieved from http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-40692

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Schulte, Kathrin. “NO/cGMP-vermittelte Signaltransduktion : Aufklärung der direkten und indirekten Interaktion mit kontraktilen Faktoren innerhalb der Gefäßregulation.” 2012. Thesis, Ruhr Universität Bochum. Accessed March 03, 2021. http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-40692.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Schulte, Kathrin. “NO/cGMP-vermittelte Signaltransduktion : Aufklärung der direkten und indirekten Interaktion mit kontraktilen Faktoren innerhalb der Gefäßregulation.” 2012. Web. 03 Mar 2021.

Vancouver:

Schulte K. NO/cGMP-vermittelte Signaltransduktion : Aufklärung der direkten und indirekten Interaktion mit kontraktilen Faktoren innerhalb der Gefäßregulation. [Internet] [Thesis]. Ruhr Universität Bochum; 2012. [cited 2021 Mar 03]. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-40692.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Schulte K. NO/cGMP-vermittelte Signaltransduktion : Aufklärung der direkten und indirekten Interaktion mit kontraktilen Faktoren innerhalb der Gefäßregulation. [Thesis]. Ruhr Universität Bochum; 2012. Available from: http://nbn-resolving.de/urn/resolver.pl?urn=urn:nbn:de:hbz:294-40692

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

9. McCollum, LaTronya. The Role of Angiotensin-(1-7) in the Modulation of Angiotensin II-Dependent Cardiac Remodeling.

Degree: 2009, Wake Forest University

URL: http://hdl.handle.net/10339/14858

► Cardiac remodeling with associated changes in myocardial structure and function occurs in response to injury to the heart concomitant with chronic hypertension. The structural changes… (more)

▼ Cardiac remodeling with associated changes in myocardial structure and function occurs in response to injury to the heart concomitant with chronic hypertension. The structural changes to the heart, including myocyte and vascular hypertrophy as well as interstitial and perivascular fibrosis, are attributed to a combination of both hemodynamic and humoral factors, such as angiotensin II (Ang II). Angiotensin-(1-7) [Ang-(1-7)] is an endogenous heptapeptide of the renin-angiotensin system with anti-proliferative properties which oppose the actions of Ang II. The purpose of this study was to determine whether Ang-(1-7) inhibits the Ang II-mediated growth of cardiac cells in vivo and in vitro and identify the molecular mechanisms for the inhibition of cardiac cell growth. Rats were treated with Ang II, in the presence or absence of Ang-(1-7), to determine the effect of the heptapeptide on Ang II-mediated cardiac myocyte hypertrophy, fibrosis and vascular hypertrophy. Subcutaneous infusion of Ang II (24 g/kg/h) for 28 days into male Sprague-Dawley rats increased systolic blood pressure (174.7 ± 6.3 mmHg), compared to saline-infused animals (125.8 ± 4.5 mmHg, n = 6, p < 0.01) or rats infused with Ang-(1-7) alone (s.c., 24 g/kg/h for 28 days; 127.4 ± 3.7, n = 6); however, co-treatment with Ang-(1-7) did not alter the Ang II-induced increase in blood pressure (168.3 ± 8.3 mmHg). Microscopic evaluation of cardiac myocyte cross-sectional area (MCSA) showed that Ang II significantly increased MCSA (33%) compared to saline- infused controls, while co-infusion of Ang-(1-7) significantly prevented the Ang II-mediated increase in MCSA (p < 0.001). In addition, hearts of animals infused with Ang II showed a marked increase in atrial natriuretic peptide (ANP) mRNA (3.76 ± 0.53) and brain natiruretic peptide (BNP) mRNA, markers of cardiac hypertrophy, compared to saline-infused animals (1.02 ± 0.06). Concomitant treatment with Ang-(1-7) significantly attenuated the increase in ANP and BNP mRNA (1.043 ± 0.11). These data indicate that the heptapeptide attenuates cardiac myocyte hypertrophy in this hypertensive model. Our previous studies demonstrated that Ang-(1-7) reduces the growth of cardiac myocytes in vitro, in association with a reduction in ERK1/ERK2 mitogen-activated protein (MAP) kinase activities. Ang II infusion significantly increased phosphorylation of ERK1/ERK2 (0.89 ± 0.45, n = 6, p < 0.05) when compared to saline-infused animals (0.18 ± 0.07). In contrast, co-infusion with Ang-(1-7) significantly decreased the Ang II-induced ERK1/ERK2 activation. (0.19 ± 0.11). Previous studies demonstrated that stimulation of MAP kinases is associated with cardiac hypertrophy while over-expression of the MAP kinase phosphatase MKP-1 (the dual-specificity phosphatase, DUSP-1) reduced cardiac hypertrophy. Ang-(1-7) significantly increased DUSP-1 protein expression in the heart (2.64 ± 0.68, n = 6, p < 0.05) compared to animals treated with saline (0.90 ±.0.30). Co-infusion of Ang II and Ang-(1-7) markedly enhanced the…

Subjects/Keywords: Angiotensin II

…Angiotensin System 20 Local Renin-Angiotensin Systems 25 Cardiovascular Regulation by Ang II 32… …CHAPTER II Angiotensin-(1-7) Attenuates Angiotensin II-Induced Cardiac Hypertrophy… …myocyte cross-sectional area 132 CHAPTER II Figure 3 Angiotensin peptides alter atrial… …Converting Enzyme ACE2 Angiotensin Converting Enzyme 2 Ang I Angiotensin I Ang II Angiotensin… …II Ang-(1-7) Angiotensin-(1-7) APS Ammonium persulfate AT(1-7…

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APA (6^th Edition):

McCollum, L. (2009). The Role of Angiotensin-(1-7) in the Modulation of Angiotensin II-Dependent Cardiac Remodeling. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/14858

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

McCollum, LaTronya. “The Role of Angiotensin-(1-7) in the Modulation of Angiotensin II-Dependent Cardiac Remodeling.” 2009. Thesis, Wake Forest University. Accessed March 03, 2021. http://hdl.handle.net/10339/14858.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

McCollum, LaTronya. “The Role of Angiotensin-(1-7) in the Modulation of Angiotensin II-Dependent Cardiac Remodeling.” 2009. Web. 03 Mar 2021.

Vancouver:

McCollum L. The Role of Angiotensin-(1-7) in the Modulation of Angiotensin II-Dependent Cardiac Remodeling. [Internet] [Thesis]. Wake Forest University; 2009. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10339/14858.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

McCollum L. The Role of Angiotensin-(1-7) in the Modulation of Angiotensin II-Dependent Cardiac Remodeling. [Thesis]. Wake Forest University; 2009. Available from: http://hdl.handle.net/10339/14858

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

10. Pendergrass, Karl Dean II. Sex-Related Differences in Hypertension and Renal Injury: Role of the Renin-Angiotensin System.

Degree: 2009, Wake Forest University

URL: http://hdl.handle.net/10339/14695

► Sex differences in hypertension and tissue injury are evident in experimental models and human subjects, yet the mechanisms underlying this disparity remain equivocal. The prevalence… (more)

▼ Sex differences in hypertension and tissue injury are evident in experimental models and human subjects, yet the mechanisms underlying this disparity remain equivocal. The prevalence of hypertension in the United States has increased over the past century and progresses at a faster rate in men than in premenopausal women. The renin-angiotensin system (RAS) contributes to the development and maintenance of hypertension. Angiotensin II (Ang II) and angiotensin-(1-7) are two peptides derived from the RAS that possess vasoconstrictive and vasodilatory actions, respectively. Ang II contributes to hypertension and effective antihypertensive treatments involve enzyme inhibition and receptor blockade to prevent the effects of Ang II. Estrogen may provide a protective effect in women because the hormone exerts an inhibitory action on Ang II production and activity. Therefore, the current studies sought to define the extent of female-male differences in the circulating and renal RAS of the mRen(2).Lewis, a monogenetic model of Ang II-dependent hypertension that overexpresses the mouse renin 2 (Ren-2) gene, and the control Lewis rats. Male mRen(2).Lewis rats have significantly higher blood pressure, plasma and renal Ang II than male Lewis rats. Furthermore, mRen(2).Lewis rats also exhibit a marked sex difference both in the extent of hypertension and Ang II that is not present in the Lewis strain. Plasma renin, angiotensin converting enzyme (ACE), and Ang I are lower in female mRen(2).Lewis as compared to male mRen(2).Lewis rats. In association with lower blood pressure, female mRen(2).Lewis expressed greater Ang-(1-7) suggesting a protective vasodilatory mechanism. Moreover, evaluation of the intrarenal RAS revealed a similar sex difference in the RAS of the mRen(2).Lewis that was not present in the Lewis strain. Renal Ang II was lower, while cortical neprilysin, an enzyme that degrades Ang II and generates Ang-(1-7) from Ang I, was significantly higher in female versus male mRen(2).Lewis. Neprilysin is stimulated by estrogen and may contribute to lower blood pressure through the renal metabolism of Ang II, as well as the formation of Ang-(1-7). Therefore, we determined whether chronic administration of the neprilysin inhibitor SCH 39370 would increase blood pressure and Ang II levels in female mRen(2).Lewis rats. Following a two week treatment, blood pressure was significantly decreased by 20 mm Hg. Neither circulating nor urinary Ang II and Ang-(1-7) levels were altered by neprilysin inhibition. In conclusion, our studies revealed that the increased expression of renal neprilysin in the female mRen(2).Lewis rat does not contribute to the sex-dependent difference in blood pressure for this model of hypertension.

Subjects/Keywords: Angiotensin II

…Angiotensin Converting Enzyme 2 AT1 Angiotensin II type 1 receptor AT2 Angiotensin II type 2… …contributes to the development and maintenance of hypertension. Angiotensin II (Ang II)… …apparatus cells of the kidneys. Ang I is then hydrolyzed to Ang II by angiotensin converting… …30 Figure 2: Enzymatic Pathway of the Renin-Angiotensin System (RAS)......32… …Figure 3: Regulatory actions of sex steroids on the Renin-Angiotensin System (RAS)…

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APA (6^th Edition):

Pendergrass, K. D. I. (2009). Sex-Related Differences in Hypertension and Renal Injury: Role of the Renin-Angiotensin System. (Thesis). Wake Forest University. Retrieved from http://hdl.handle.net/10339/14695

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Pendergrass, Karl Dean II. “Sex-Related Differences in Hypertension and Renal Injury: Role of the Renin-Angiotensin System.” 2009. Thesis, Wake Forest University. Accessed March 03, 2021. http://hdl.handle.net/10339/14695.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Pendergrass, Karl Dean II. “Sex-Related Differences in Hypertension and Renal Injury: Role of the Renin-Angiotensin System.” 2009. Web. 03 Mar 2021.

Vancouver:

Pendergrass KDI. Sex-Related Differences in Hypertension and Renal Injury: Role of the Renin-Angiotensin System. [Internet] [Thesis]. Wake Forest University; 2009. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10339/14695.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Pendergrass KDI. Sex-Related Differences in Hypertension and Renal Injury: Role of the Renin-Angiotensin System. [Thesis]. Wake Forest University; 2009. Available from: http://hdl.handle.net/10339/14695

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Queens University

11. Latchford, Kevin Jason. Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat .

Degree: Physiology, 2008, Queens University

URL: http://hdl.handle.net/1974/995

► The role of the hypothalamic paraventricular nucleus (PVN) in cardiovascular and neuroendocrine regulation has been well documented. Much remains unknown however about the integration of… (more)

▼ The role of the hypothalamic paraventricular nucleus (PVN) in cardiovascular and neuroendocrine regulation has been well documented. Much remains unknown however about the integration of synaptic signals within this nucleus and the neuronal subtypes and chemical messengers governing these processes. Angiotensin II (ANG) has been demonstrated to act as a neurotransmitter in PVN where it exerts considerable influence on neuronal excitability. The studies within this thesis were undertaken to delineate the actions of ANG on the membrane properties of PVN neurons and its effect on synaptic transmission within this nucleus. We report that ANG activates a nitric oxide mediated negative feedback loop in the PVN. The magnitude of the depolarizing response to ANG appears to be dependant on this GABAergic inhibitory input demonstrating there exists within PVN an intrinsic negative feedback loop which modulates neuronal excitability in response to peptidergic excitation. We also demonstrate that the depolarizing response to ANG in magnocellular neurons is in part dependent upon increases in glutamatergic excitatory synaptic input. These data in combination highlight the multiple levels of synaptic integration controlling the output of magnocellular neurons in PVN. PVN also contains significant populations of neurosecretory parvocellular neurons which exercise considerable influence over the adenohypophysis and therefore neuroendocrine regulation. ANG caused an AT1 receptor mediated depolarization of these neurosecretory neurons. Voltage-clamp analysis revealed that ANG activated a non-selective cationic current and reduced a sustained potassium current characteristic of IK. These studies identify multiple post-synaptic modulatory sites through which ANG can influence the excitability of neurosecretory parvocellular PVN neurons. The findings in this thesis provide the framework for a cellular model of action of ANG within PVN to regulate the activity of this nucleus not only through direct cellular mediated ion channel interactions but also through modulation of synaptic input within the magnocellular system of PVN.

Subjects/Keywords: PVN ; Angiotensin II

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APA (6^th Edition):

Latchford, K. J. (2008). Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat . (Thesis). Queens University. Retrieved from http://hdl.handle.net/1974/995

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Latchford, Kevin Jason. “Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat .” 2008. Thesis, Queens University. Accessed March 03, 2021. http://hdl.handle.net/1974/995.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Latchford, Kevin Jason. “Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat .” 2008. Web. 03 Mar 2021.

Vancouver:

Latchford KJ. Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat . [Internet] [Thesis]. Queens University; 2008. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1974/995.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Latchford KJ. Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat . [Thesis]. Queens University; 2008. Available from: http://hdl.handle.net/1974/995

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Virginia Tech

12. Wahlberg, Kristin. The Role of Angiotensin II in Skeletal Muscle Metabolism.

Degree: MS, Human Nutrition, Foods, and Exercise, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/42504

► Hypertension and diabetes have long been closely linked. As such, the major player in the renin, angiotensin system, angiotensin II, has recently been investigated for… (more)

Subjects/Keywords: ROS; oxidation; skeletal muscle; angiotensin II

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APA (6^th Edition):

Wahlberg, K. (2011). The Role of Angiotensin II in Skeletal Muscle Metabolism. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/42504

Chicago Manual of Style (16^th Edition):

Wahlberg, Kristin. “The Role of Angiotensin II in Skeletal Muscle Metabolism.” 2011. Masters Thesis, Virginia Tech. Accessed March 03, 2021. http://hdl.handle.net/10919/42504.

MLA Handbook (7^th Edition):

Wahlberg, Kristin. “The Role of Angiotensin II in Skeletal Muscle Metabolism.” 2011. Web. 03 Mar 2021.

Vancouver:

Wahlberg K. The Role of Angiotensin II in Skeletal Muscle Metabolism. [Internet] [Masters thesis]. Virginia Tech; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10919/42504.

Council of Science Editors:

Wahlberg K. The Role of Angiotensin II in Skeletal Muscle Metabolism. [Masters Thesis]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/42504

13. Giaquinto, Luciana dos Reis Rigueiral. Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional.

Degree: Mestrado, Farmacologia, 2011, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-12082011-154406/ ;

►

O objetivo deste estudo foi avaliar se a infusão de angiotensina II (ANG II) modulava a expressão do receptor B1 (RB1) de cininas em aorta… (more)

▼

O objetivo deste estudo foi avaliar se a infusão de angiotensina II (ANG II) modulava a expressão do receptor B1 (RB1) de cininas em aorta (AO),arteríolas mesentéricas (AM) de ratos Wistar e também verificar a influência do RB1 na pressão arterial e reatividade desses vasos sanguíneos através do agonista de RB1, DABK. Os ratos receberam por 28 dias infusão de ANG II ou de ANG II e antagonista de RB1. O DABK induziu relaxamento dependente de endotélio e NO em anéis de AO de ratos ANG II. A infusão de ANG II causou hipertensão arterial, aumento da expressão de RNAm de RB1 em AO e AM, da expressão protéica de RB1 em AO e disfunção endotelial caracterizada por diminuída resposta á acetilcolina (ACH).O antagonista de B1R não interferiu no desenvolvimento de hipertensão e na disfunção endotelial causada, mas aumentou a sensibilidade da AO à ACH e a expressão de NO Sintase nos ratos ANG II. Esses resultados nos permitem sugerir que a ANG II e cininas podem atuar sinergicamente no desenvolvimento das alterações vasculares observadas nesse modelo de hipertensão arterial.

The aim of the present study was to evaluate whether the angiotensin II (ANG II) infusion modulates the kinin B1 receptor (B1R) mRNA, protein expression in aorta (AO) and mesenteric arterioles (MA) in Wistar rats. It was also verified the role of RB1 in the control of blood pressure and vascular reactivity using DABK a B1R agonist Rats were infused either with ANG II (400ng/Kg/min) or ANG II plus RB1antagonist(350ng/Kg/min) during 28 days.DABK induced endothelium-NO dependent relaxation in AO of ANG II rats. ANG II infusion caused hypertension, increased RB1 mRNA expression in AO and MA, protein expression in AO and caused endothelial dysfunction, characterized as a decreased maximal response to acetylcholine (ACH). The B1R antagonist did not interfere in the development of hypertension and endothelium dysfunction caused by ANG II, however, increased the sensitivity to ACH and NO synthase expression in AO of ANG II rats. Altogether, we may suggest that ANG II and kinins can act synergistically in the development of vascular changes in this model of hypertension.

Advisors/Committee Members: Carvalho, Maria Helena Catelli de.

Subjects/Keywords: Angiotensin II; Angiotensin receptors; Angiotensina II; Cininas; Hipertensão; Hypertension; Kinins; Receptores de angiotensina; Renin-angiotensin; Sistema renina-angiotensina

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Giaquinto, L. d. R. R. (2011). Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42136/tde-12082011-154406/ ;

Chicago Manual of Style (16^th Edition):

Giaquinto, Luciana dos Reis Rigueiral. “Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional.” 2011. Masters Thesis, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-12082011-154406/ ;.

MLA Handbook (7^th Edition):

Giaquinto, Luciana dos Reis Rigueiral. “Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional.” 2011. Web. 03 Mar 2021.

Vancouver:

Giaquinto LdRR. Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional. [Internet] [Masters thesis]. University of São Paulo; 2011. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-12082011-154406/ ;.

Council of Science Editors:

Giaquinto LdRR. Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional. [Masters Thesis]. University of São Paulo; 2011. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-12082011-154406/ ;

14. Akashi, Ana Eliza. Caracterização de um sistema renina-angiotensina local no tecido gengival de rato.

Degree: PhD, Biologia Oral, 2008, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/25/25142/tde-13032009-094618/ ;

►

O sistema renina-angiotensina (SRA) circulante é um sistema endócrino que promove a produção de angiotensina (Ang) II, a qual exerce seus efeitos pela interação com… (more)

▼

O sistema renina-angiotensina (SRA) circulante é um sistema endócrino que promove a produção de angiotensina (Ang) II, a qual exerce seus efeitos pela interação com receptores específicos. O conceito clássico do SRA circulante está sendo modificado, pois tem sido demonstrada a existência de sistemas locais capazes de gerar angiotensinas de forma independente do SRA circulante em vários tecidos e órgãos. Trabalhos recentes sugerem a existência de alguns componentes do SRA em tecido gengival e fibroblastos gengivais de diferentes espécies. Porém, não são encontrados na literatura achados inequívocos sobre a presença de importantes componentes do SRA, tais como renina e angiotensinogênio, no tecido gengival de rato. Portanto, os objetivos do presente trabalho foram: 1) estudar a expressão e localização de componentes do SRA no tecido gengival de rato e 2) estudar in vitro a funcionalidade do SRA local em homogenato de tecido gengival de rato quanto à formação de Ang II e outros peptídeos vasoativos a partir de precursores de Ang II. Transcrição reversa seguida de reação em cadeia da polimerase (RTPCR) foi utilizada para avaliar a expressão de RNAm. Análise imunohistoquímica foi utilizada para detecção e localização de renina no tecido gengival de rato. Um método fluorimétrico padronizado com o tripeptídeo Hipuril-Histidina-Leucina (Hip-His-Leu) foi usado para medir a atividade da ECA em homogenatos de tecido gengival de rato. A técnica de cromatografia líqüida de alto desempenho (HPLC) foi usada para analisar os produtos formados após a incubação de homogenatos de tecido gengival de rato com Ang I ou tetradecapeptídeo substrato de renina (TDP). RT-PCR revelou a expressão de RNAm para renina, angiotensinogênio, ECA e receptores de Ang II (AT1a, AT1b e AT2) em tecido gengival; em fibroblastos cultivados de tecido gengival foi observada expressão de RNAm para renina, angiotensinogênio e receptor AT1a. A técnica de imunohistoquímica demonstrou a existência de renina em vasos de tecido gengival de rato. Atividade da ECA foi detectada por meio do ensaio fluorimétrico (4,95±0,89 nmol His-Leu/g.min). Quando Ang I foi usada como substrato, análises de HPLC mostraram a formação de Ang 1-9 (0,576±0,128 nmol/mg.min), Ang II (0,066±0,008 nmol/mg.min) e Ang 1-7 (0,111±0,017 nmol/mg.min), enquanto que os mesmos peptídeos (0,139±0,031; 0,206±0,046 e 0,039±0,007 nmol/mg.min, respectivamente) e Ang I (0,973±0,139 nmol/mg.min) foram formados quando TDP foi usado como substrato. Adicionalmente, análises de HPLC revelaram a ausência de enzimas que degradam Ang II em homogenatos de tecido gengival de rato. Em conclusão, os resultados apresentados neste trabalho mostram claramente a existência de um SRA local em tecido gengival de rato, que é capaz de gerar Ang II e outros peptídeos vasoativos in vitro. Estudos adicionais são necessários para elucidar o papel deste sistema local no tecido gengival de rato.

Systemic renin-angiotensin system (RAS) promotes the plasmatic production of angiotensin (Ang) II, which acts through the interaction…

Advisors/Committee Members: Santos, Carlos Ferreira dos.

Subjects/Keywords: Angiotensin I; Angiotensin II; Angiotensin receptors; Angiotensin-converting enzyme; Angiotensina I; Angiotensina II; Angiotensinogen; Angiotensinogênio; Enzima conversora de angiotensina; Receptores de angiotensina; Renin; Renin-angiotensin system; Renina; Sistema renina-angiotensina

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Akashi, A. E. (2008). Caracterização de um sistema renina-angiotensina local no tecido gengival de rato. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/25/25142/tde-13032009-094618/ ;

Chicago Manual of Style (16^th Edition):

Akashi, Ana Eliza. “Caracterização de um sistema renina-angiotensina local no tecido gengival de rato.” 2008. Doctoral Dissertation, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/25/25142/tde-13032009-094618/ ;.

MLA Handbook (7^th Edition):

Akashi, Ana Eliza. “Caracterização de um sistema renina-angiotensina local no tecido gengival de rato.” 2008. Web. 03 Mar 2021.

Vancouver:

Akashi AE. Caracterização de um sistema renina-angiotensina local no tecido gengival de rato. [Internet] [Doctoral dissertation]. University of São Paulo; 2008. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/25/25142/tde-13032009-094618/ ;.

Council of Science Editors:

Akashi AE. Caracterização de um sistema renina-angiotensina local no tecido gengival de rato. [Doctoral Dissertation]. University of São Paulo; 2008. Available from: http://www.teses.usp.br/teses/disponiveis/25/25142/tde-13032009-094618/ ;

15. Canale, Daniele. Inibição do sistema NF-KB durante a lactação promove hipertensão na vida adulta.

Degree: Mestrado, Nefrologia, 2009, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5148/tde-03022010-145914/ ;

►

Em roedores, a administração de Losartan (LO) durante a nefrogênese (primeiras duas semanas de vida) leva à insuficiência renal progressiva e, mais tardiamente, à hipertensão,… (more)

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Em roedores, a administração de Losartan (LO) durante a nefrogênese (primeiras duas semanas de vida) leva à insuficiência renal progressiva e, mais tardiamente, à hipertensão, indicando que a Angiotensina II (AII) é indispensável a uma nefrogênese adequada. Os mediadores intracelulares desse efeito são desconhecidos. Nós investigamos se o sistema NF-kB, que tem influência na embriogênese de outros tecidos, poderia ser um desses mediadores. Trinta e duas ratas Munich Wistar, cada uma amamentando 6 filhotes, foram divididas em dois grupos: C, sem tratamento, e PDTC, que receberam o inibidor do NF-kB Pirrolidina Ditiocarbamato (PDTC), 280 mg/kg/dia na água de beber durante 21 dias. A prole (C e PDTC), constituída de ratos machos, foi acompanhada até 10 meses de vida sem qualquer tratamento. Diferentemente do observado anteriormente com o LO, o PDTC não promoveu redução do número de néfrons nem albuminúria, indicando que o sistema NF-kB não participa crucialmente da nefrogênese. No entanto, os ratos que receberam o PDTC durante a lactação apresentaram hipertensão persistente, associada a hipertrofia de miócitos e a fibrose miocárdica. Para investigar a patogênese da hipertensão (que não se pode explicar por uma redução no número de néfrons), as expressões renais dos componentes do sistema renina-angiotensina (SRA) e dos transportadores tubulares foram determinadas por PCR em tempo real (qRT-PCR) aos 3 e 10 meses de vida. Aos 3 meses, a expressão de angiotensinogênio (AGT) e renina foram significativamente aumentadas no grupo PDTC vs C, indicando que uma ativação local do SRA pode explicar o desenvolvimento da hipertensão no grupo PDTC. No entanto, a expressão de todos os componentes do SRA examinados nos animais que receberam o PDTC durante a nefrogênese estava diminuída aos 10 meses, possivelmente devido a um mecanismo compensatório, sugerindo que a hipertensão foi mantida por outros mecanismos. No túbulo proximal, observou-se um aumento da expressão do transportador sódio/glicose isoforma 1 (SGLT1) (luminal) e sódio/bicarbonato (NBC) (basolateral), bem como um aumento numérico na expressão do trocador luminal sódio/hidrogênio isoforma 3 (NHE3), sugerindo que essas anormalidades podem estar envolvidas na patogênese da hipertensão nesses animais. Aos 10 meses, a expressão de todas as moléculas estava diminuída, sugerindo a participação de outros mecanismos na manutenção da hipertensão em longo prazo. A administração de PDTC pode representar um novo modelo de hipertensão essencial, possivelmente iniciada pela ativação local do SRA e por anormalidades no transporte de sódio no túbulo proximal e mantida em longo prazo por outros mecanismos.

Losartan treatment during late murine nephrogenesis (first 2 weeks of extrauterine life) causes progressive renal injury in adult life and, at more advanced stages, hypertension, indicating a physiologic action of angiotensin II on nephrogenesis. The possible intracellular pathways that might mediate this effect are unknown. We investigated the possibility that the NF-kB system, known…

Advisors/Committee Members: Zatz, Roberto.

Subjects/Keywords: Angiotensin II; Angiotensina II; Hipertensão; Hypertension; NF-kB; NF-kB

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Canale, D. (2009). Inibição do sistema NF-KB durante a lactação promove hipertensão na vida adulta. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5148/tde-03022010-145914/ ;

Chicago Manual of Style (16^th Edition):

Canale, Daniele. “Inibição do sistema NF-KB durante a lactação promove hipertensão na vida adulta.” 2009. Masters Thesis, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/5/5148/tde-03022010-145914/ ;.

MLA Handbook (7^th Edition):

Canale, Daniele. “Inibição do sistema NF-KB durante a lactação promove hipertensão na vida adulta.” 2009. Web. 03 Mar 2021.

Vancouver:

Canale D. Inibição do sistema NF-KB durante a lactação promove hipertensão na vida adulta. [Internet] [Masters thesis]. University of São Paulo; 2009. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5148/tde-03022010-145914/ ;.

Council of Science Editors:

Canale D. Inibição do sistema NF-KB durante a lactação promove hipertensão na vida adulta. [Masters Thesis]. University of São Paulo; 2009. Available from: http://www.teses.usp.br/teses/disponiveis/5/5148/tde-03022010-145914/ ;

16. Dias, Ana Alice dos Santos. Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase.

Degree: PhD, Farmacologia, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;

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As espécies reativas de oxigênio (EROs) são intermediários de vias de sinalização que regulam eventos celulares relevantes na função de células musculares lisas vasculares como… (more)

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As espécies reativas de oxigênio (EROs) são intermediários de vias de sinalização que regulam eventos celulares relevantes na função de células musculares lisas vasculares como migração, proliferação e contração. A NADPH oxidase é a principal fonte enzimática de EROs com finalidade sinalizadora no sistema cardiovascular. Estudos do nosso grupo demonstraram que a proteína dissulfeto isomerase (PDI), uma chaperona redox do retículo endoplasmåtico é capaz de modular a geração de EROs e a ativação de vias de sinalização redox dependentes pela Ang II. Apesar dos recentes avanços na compreensão dos mecanismos que regulam a interação entre a PDI e NADPH oxidase, o papel desta chaperona nos efeitos biológicos relacionados a EROs, como a contração vascular, não estão esclarecidos. A inibição da resposta contrátil pelo DTNB, um oxidante de tióis sugere o envolvimento de proteínas contendo tióis como a PDI e a NADPH oxidase na contração de aortas isoladas estimuladas com Ang II. Estes resultados foram confirmados por experimentos que demonstraram a expressão de PDI em todas as camadas vasculares da aorta de ratos Wistar e uma co-localização desta proteína com a isoforma NOX-1. A inibição da PDI diminuiu a geração de EROs e a reatividade vascular induzida por Ang II e NOR independente da presença do endotélio. A investigação dos mecanismos envolvidos sugere um papel da PDI na mobilização de cálcio dos estoques intracelulares via NADPH oxidase. A ativação de MAP quinases contribuiu para aumentar a mobilização de cálcio intracelular em aortas estimuladas com Ang II e NOR. No entanto, a inibição da PDI reduziu a fosforilação da ERK 1/2 em aortas estimuladas com Ang II, mas não com NOR. A análise conjunta dos nossos resultados sugere que mecanismos redox dependentes e independentes estariam envolvidos na regulação da resposta contrátil à Ang II e NOR pela PDI.

The reactive oxygen species (ROS) are intermediates of signaling pathways which regulates cellular events relevant for the vascular smooth cells function as migration, proliferation and contraction.The NADPH oxidase is the main enzimatic source of ROS with the signaling purpose on the cardiovascular system. We previously demonstrated that the protein disulfide isomerase (PDI), a redox chaperone of endoplasmic reticulum, is able to modulate the ROS generation and the activation of signaling redox ways dependent of Ang II. Although the recent advances in the understanding of mechanisms that regulate the interaction of PDI and NADPH oxidase, the role of this chaperone in the biological effects related to ROS, as vascular contraction, are not well clarified. The inhibition of the contractile response by DTNB, an oxidant thiol, suggest the involvement of proteins containing thiols as the PDI and NADPH oxidase in the contraction of isolated aortas stimulated with Ang II. These results were confirmed by experiments that demonstrated the PDI expression in Wistar rats vascular layers and a co-localization of this protein with the NOX-1 isoform. The PDI inhibition decreased ROS…

Advisors/Committee Members: Lopes, Lucia Rossetti.

Subjects/Keywords: Angiotensin II; Angiotensina II; Noradrenalina; Norepinephrine; Protein; Proteínas

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Dias, A. A. d. S. (2012). Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;

Chicago Manual of Style (16^th Edition):

Dias, Ana Alice dos Santos. “Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase.” 2012. Doctoral Dissertation, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;.

MLA Handbook (7^th Edition):

Dias, Ana Alice dos Santos. “Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase.” 2012. Web. 03 Mar 2021.

Vancouver:

Dias AAdS. Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase. [Internet] [Doctoral dissertation]. University of São Paulo; 2012. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;.

Council of Science Editors:

Dias AAdS. Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase. [Doctoral Dissertation]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;

Universidade Federal de Mato Grosso do Sul

17. Muzili, Nayara de Araujo. Influência do bloqueio de receptor de angiotensina II na modulação do fenótipo muscular esquelético em ratos submetidos à dieta hiperlipídica .

Degree: 2016, Universidade Federal de Mato Grosso do Sul

URL: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2748

► INTRODUÇÃO: Alterações musculares foram verificadas em estudos clínicos e experimentais sobre obesidade. Há evidência que a angiotensina II (AngII) está aumentada sistemicamente na obesidade, porém… (more)

▼ INTRODUÇÃO: Alterações musculares foram verificadas em estudos clínicos e experimentais sobre obesidade. Há evidência que a angiotensina II (AngII) está aumentada sistemicamente na obesidade, porém o seu papel na modulação de modificações musculares na obesidade ainda não foi elucidado. OBJETIVO: Avaliar a influência do bloqueio do receptor de angiotensina II sobre vias sinalizadoras envolvidas na modulação do fenótipo muscular em ratos submetidos à dieta hiperlipídica. MATERIAIS E MÉTODOS : Ratos Wistar machos (n=48, 30 dias de idade) foram distribuídos em dois grupos: C e DH. O grupo controle (C) foi tratado com dieta normocalórica e os animais do grupo DH com dieta hiperlipídica. O período experimental teve duração de 20 semanas. Na 16ª semana, cada grupo foi subdividido: C e C+Lo s; DH e DH+Los. Os grupos C e DH continuaram recebendo as respectivas dietas durante mais quatro semanas. Os grupos C+Los e DH+Los, além do suporte nutricional, foram tratados com losartan (30 mg/kg/dia). Foram realizadas as seguintes análises dos músculos sóleo e gastrocnêmio (porção branca): mensuração da área seccional transversa das fibras musculares, quantificação da fração intersticial de colágeno, avaliação da expressão proteica do receptor AT1 e de JNK. RESULTADOS: Os animais alimentados com dieta hiperlipídica apresentaram aumento da área seccional transversa das fibras do músculo gastrocnêmio, associado à diminuição da ativação da JNK e aumento na expressão dos receptores AT1. O losartan reduziu a expressão de AT1 nos músculo sóleo e gastrocnêmio e reduziu a fração intersticial de colágeno no músculo sóleo no grupo alimentado com dieta hiperlipídica. CONCLUSÕES: O consumo de dieta hiperlipídica está associado com alterações morfológicas e moleculares na musculatura esquelética, porém de forma diferenciada em músculos com predominância de fibras lentas ou de fibras rápidas. Ademais, essas alterações são parcialmente moduladas pela angiotensina II. Advisors/Committee Members: Martinez, Paula Felippe (advisor).

Subjects/Keywords: Obesidade; Músculos Esqueléticos; Angiotensina II; Obesity; Striated Muscle; Angiotensin II

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Muzili, N. d. A. (2016). Influência do bloqueio de receptor de angiotensina II na modulação do fenótipo muscular esquelético em ratos submetidos à dieta hiperlipídica . (Thesis). Universidade Federal de Mato Grosso do Sul. Retrieved from http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2748

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Muzili, Nayara de Araujo. “Influência do bloqueio de receptor de angiotensina II na modulação do fenótipo muscular esquelético em ratos submetidos à dieta hiperlipídica .” 2016. Thesis, Universidade Federal de Mato Grosso do Sul. Accessed March 03, 2021. http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2748.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Muzili, Nayara de Araujo. “Influência do bloqueio de receptor de angiotensina II na modulação do fenótipo muscular esquelético em ratos submetidos à dieta hiperlipídica .” 2016. Web. 03 Mar 2021.

Vancouver:

Muzili NdA. Influência do bloqueio de receptor de angiotensina II na modulação do fenótipo muscular esquelético em ratos submetidos à dieta hiperlipídica . [Internet] [Thesis]. Universidade Federal de Mato Grosso do Sul; 2016. [cited 2021 Mar 03]. Available from: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2748.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Muzili NdA. Influência do bloqueio de receptor de angiotensina II na modulação do fenótipo muscular esquelético em ratos submetidos à dieta hiperlipídica . [Thesis]. Universidade Federal de Mato Grosso do Sul; 2016. Available from: http://repositorio.cbc.ufms.br:8080/jspui/handle/123456789/2748

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

18. Μακρυγιαννάκης, Γεώργιος. Αιμοδυναμική μελέτη της αγγειοτενσίνης ΙΙ και των αναλογών της σε κουνέλια.

Degree: 1998, Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); Democritus University of Thrace (DUTH)

URL: http://hdl.handle.net/10442/hedi/11462

Subjects/Keywords: Αγγειοτενσίνη II; Κουνέλια; Angiotensin II

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Μακρυγιαννάκης, �. (1998). Αιμοδυναμική μελέτη της αγγειοτενσίνης ΙΙ και των αναλογών της σε κουνέλια. (Thesis). Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); Democritus University of Thrace (DUTH). Retrieved from http://hdl.handle.net/10442/hedi/11462

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Μακρυγιαννάκης, Γεώργιος. “Αιμοδυναμική μελέτη της αγγειοτενσίνης ΙΙ και των αναλογών της σε κουνέλια.” 1998. Thesis, Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); Democritus University of Thrace (DUTH). Accessed March 03, 2021. http://hdl.handle.net/10442/hedi/11462.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Μακρυγιαννάκης, Γεώργιος. “Αιμοδυναμική μελέτη της αγγειοτενσίνης ΙΙ και των αναλογών της σε κουνέλια.” 1998. Web. 03 Mar 2021.

Vancouver:

Μακρυγιαννάκης �. Αιμοδυναμική μελέτη της αγγειοτενσίνης ΙΙ και των αναλογών της σε κουνέλια. [Internet] [Thesis]. Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); Democritus University of Thrace (DUTH); 1998. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10442/hedi/11462.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Μακρυγιαννάκης �. Αιμοδυναμική μελέτη της αγγειοτενσίνης ΙΙ και των αναλογών της σε κουνέλια. [Thesis]. Δημοκρίτειο Πανεπιστήμιο Θράκης (ΔΠΘ); Democritus University of Thrace (DUTH); 1998. Available from: http://hdl.handle.net/10442/hedi/11462

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

19. Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki, Kenichiro. Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development. : 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク.

Degree: 博士（医学）, 2018, Nara Medical University / 奈良県立医科大学

URL: http://hdl.handle.net/10564/3429

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Periostin is a 90‑kDa extracellular matrix protein, which is secreted primarily from fibroblasts and is expressed in the lungs, kidneys and heart valves. Angiotensin II… (more)

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Periostin is a 90‑kDa extracellular matrix protein, which is secreted primarily from fibroblasts and is expressed in the lungs, kidneys and heart valves. Angiotensin II (AT‑II) serves pivotal roles in the pathogenesis of several diseases with accompanying fibrosis, including chronic liver diseases. AT‑II induces periostin expression by regulating transforming growth factor‑β1 (TGF‑β1)/Smad signaling during cardiac fibrosis. The aim of the present study was to investigate the interaction between AT‑II and periostin during liver fibrosis development. Fischer 344 rats were fed a choline‑deficient L‑amino‑acid (CDAA)‑defined diet for 12 weeks to simulate the development of steatohepatitis with liver fibrosis. Losartan, an AT‑II type I receptor blocker, was administered to inhibit the effect of AT‑II. The therapeutic effect of losartan on hepatic fibrosis development and on periostin expression was then evaluated. Several in vitro experiments were performed to examine the mechanisms underlying the interaction between AT‑II and periostin in activated hepatic stellate cells (Ac‑HSCs). Treatment with losartan suppressed the development of liver fibrosis induced by the CDAA diet, and reduced hepatic periostin expression. In addition, losartan treatment suppressed hepatic Ac‑HSC expansion and hepatic TGF‑β1 expression. In vitro analysis using LX2 HSC cells indicated that AT‑II can augment TGF‑β1 and collagen type I α1 mRNA expression via periostin expression, suggesting that the interaction between AT‑II and periostin may serve a role in liver fibrosis development. In conclusion, blockade of AT‑II‑induced periostin may suppress the progression of liver fibrosis development.

博士（医学）・乙第1413号・平成30年3月15日

Copyright: © Takeda et al. This is an open access article distributed under the terms of Creative Commons Attribution License(CC BY-NC-ND 4.0) https://creativecommons.org/licenses/by-nc-nd/4.0/.

Subjects/Keywords: periostin; angiotensin II; liver fibrosis; renin-angiotensin system; choline-supplemented amino acid

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki, K. (2018). Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development. : 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク. (Thesis). Nara Medical University / 奈良県立医科大学. Retrieved from http://hdl.handle.net/10564/3429

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki, Kenichiro. “Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development. : 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク.” 2018. Thesis, Nara Medical University / 奈良県立医科大学. Accessed March 03, 2021. http://hdl.handle.net/10564/3429.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki, Kenichiro. “Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development. : 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク.” 2018. Web. 03 Mar 2021.

Vancouver:

Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki K. Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development. : 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク. [Internet] [Thesis]. Nara Medical University / 奈良県立医科大学; 2018. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/10564/3429.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Takeda, Kosuke; Noguchi, Ryuichi; Kitade, Mitsuteru; Namisaki, Tadashi; Moriya, Kei; Kawaratani, Hideto; Okura, Yasushi; Kaji, Kosuke; Aihara, Yosuke; Douhara, Akitoshi; Nishimura, Norihisa; Sawada, Yasuhiko; Seki K. Periostin cross‑reacts with the renin‑angiotensin system during liver fibrosis development. : 肝線維化におけるペリオスチンの役割 : レニン・アンギオテンシン系とクロストーク. [Thesis]. Nara Medical University / 奈良県立医科大学; 2018. Available from: http://hdl.handle.net/10564/3429

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of New Mexico

20. Campbell, Heather. Comparison of monotherapy with angiotensin-converting enzyme inhibitors or angtiotensin receptor blockers in improving health outcomes among veteran patients with type 2 diabetes.

Degree: College of Pharmacy, 2011, University of New Mexico

URL: http://hdl.handle.net/1928/12866

► Diabetes is a world-wide epidemic; 90-95% of diabetes cases are type 2 in nature. Albuminuria and hypertension are risk factors of diabetes complications, specifically nephropathy… (more)

▼ Diabetes is a world-wide epidemic; 90-95% of diabetes cases are type 2 in nature. Albuminuria and hypertension are risk factors of diabetes complications, specifically nephropathy and cardiovascular disease. Angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) are recommended as monotherapy to reduce albuminuria and hypertension. Because of this, we sought to compare patients with type 2 diabetes (P2DM) who received neither therapy to those who received either monotherapy for end-stage renal disease (ESRD), cardio- and cerebro- vascular disease, and all-cause mortality. Additionally, because there are very limited data on comparisons between ACEI and ARB therapies, none of which compare occurrence of incident cardio- or cerebro- vascular disease or mortality, these monotherapies were compared. Moreover, because diabetes incidence is expected to increase, healthcare utilization was also analyzed. This longitudinal study followed P2DM maximally for five years. Comparisons between patients receiving neither therapy and either monotherapy were performed with multivariate logistic or negative binomial regression, while comparisons between ACEI and ARB patients were performed with propensity score weighted logistic or negative binomial regression. Compared to neither therapy, ACEI patients were associated with lower odds of ESRD, higher odds of incident cardio- or cerebro- vascular disease events, lower odds of mortality, and higher incidence rates of healthcare utilization. Treatment selection existed between ACEI and ARB monotherapies in P2DM, necessitating propensity score analysis (PSA). Fortunately, the PSA balanced between group characteristics and had substantial overlap in propensity scores between groups, allowing for precise estimates of causal interpretation. No differences were found between ACEI and ARB monotherapies for all endpoints studied. Since only associations can be found between comparisons of ACEI and ARB patients with neither patients and because ACEIs or ARBs are recommended in guidelines, significance is focused on comparisons between ACEI and ARB patients. This is the second study lasting more than a year comparing outcomes of ACEI and ARB monotherapies for nephropathy and the first study comparing ACEI and ARB monotherapies for other endpoints. This study confirms that ACEIs and ARBs have no significant difference in effects for two years mean follow-up. Until this study, similar effects have only been assumed. Advisors/Committee Members: Khan, Nasreen, Raisch, Dennis W., Borrego, Matthew E., Murata, Glen H., Sather, Mike R..

Subjects/Keywords: Non-insulin-dependent diabetes – Chemotherapy; Angiotensin converting enzyme – Inhibitors; Angiotensin II – Antagonists.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Campbell, H. (2011). Comparison of monotherapy with angiotensin-converting enzyme inhibitors or angtiotensin receptor blockers in improving health outcomes among veteran patients with type 2 diabetes. (Doctoral Dissertation). University of New Mexico. Retrieved from http://hdl.handle.net/1928/12866

Chicago Manual of Style (16^th Edition):

Campbell, Heather. “Comparison of monotherapy with angiotensin-converting enzyme inhibitors or angtiotensin receptor blockers in improving health outcomes among veteran patients with type 2 diabetes.” 2011. Doctoral Dissertation, University of New Mexico. Accessed March 03, 2021. http://hdl.handle.net/1928/12866.

MLA Handbook (7^th Edition):

Campbell, Heather. “Comparison of monotherapy with angiotensin-converting enzyme inhibitors or angtiotensin receptor blockers in improving health outcomes among veteran patients with type 2 diabetes.” 2011. Web. 03 Mar 2021.

Vancouver:

Campbell H. Comparison of monotherapy with angiotensin-converting enzyme inhibitors or angtiotensin receptor blockers in improving health outcomes among veteran patients with type 2 diabetes. [Internet] [Doctoral dissertation]. University of New Mexico; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/1928/12866.

Council of Science Editors:

Campbell H. Comparison of monotherapy with angiotensin-converting enzyme inhibitors or angtiotensin receptor blockers in improving health outcomes among veteran patients with type 2 diabetes. [Doctoral Dissertation]. University of New Mexico; 2011. Available from: http://hdl.handle.net/1928/12866

University of Iowa

21. Pena Silva, Ricardo Alfonso. Cardiovascular oxidative stress: recent findings on ACE2 And MAO.

Degree: PhD, Pharmacology, 2012, University of Iowa

URL: https://ir.uiowa.edu/etd/3366

► Oxidative stress is associated with development and progression of cardiovascular disease. Angiotensin II produces oxidative stress and endothelial dysfunction, and its actions may be… (more)

▼ Oxidative stress is associated with development and progression of cardiovascular disease. Angiotensin II produces oxidative stress and endothelial dysfunction, and its actions may be attenuated by the activity of angiotensin converting enzyme type 2 (ACE2) which converts angiotensin II to the vasoprotective peptide angiotensin (1-7). Similarly, increased oxidative stress is associated with aortic valve stenosis in humans and mice. In my thesis studies, I explore mechanisms of modulation and generation of oxidative stress in cerebral arteries and heart valves. First, I tested the hypothesis that ACE2 deficiency increases oxidative stress and vasomotor dysfunction in cerebral arteries, and examined the role of ACE2 in vascular aging. Vasomotor function was assessed in the basilar artery ex vivo of adult and old ACE2 deficient (ACE2-/y) and wild type (WT or ACE2+/y) mice. ACE2 was present, but at relatively low levels in cerebral arteries. Systolic blood pressure was similar in adult and old ACE2-/y and ACE2+/y mice. Maximal dilatation to acetylcholine was impaired in the basilar artery from adult ACE2-/y mice compared to adult ACE2+/y. In old mice, maximal vasodilatation to acetylcholine was impaired in ACE2+/y mice and severely impaired in ACE2-/y mice. The antioxidant tempol improved responses to acetylcholine in adult and old ACE2-/y and ACE2+/y mice. Nitrotyrosine staining in the basilar artery was increased in adult ACE2-/y mice and in old ACE2-/y and ACE2+/y mice relative to adult ACE2+/y, which indicates that oxidative stress was higher in cerebral arteries from ACE2 deficient mice and old mice. Expression of NADPH oxidase subunits Nox2 and p47phox, and of pro-inflammatory molecules Rcan1 and TNF alpha; was increased in cerebral arteries from old ACE2-/y and ACE2+/y mice. Additionally, I tested the hypothesis that serotonin induces oxidative stress in human heart valves, and examined mechanisms by which serotonin may increase reactive oxygen species (ROS). Superoxide (O2.-) was measured in heart valves from explanted human hearts that were not used for transplantation. Superoxide levels (lucigenin-enhanced chemiluminescence) were increased in homogenates of cardiac valves and pulmonary artery after incubation with serotonin. A non-specific inhibitor of flavin-oxidases (DPI), or inhibitors of monoamine oxidase-MAO (tranylcypromine and clorgyline), prevented serotonin-induced increase in O2.-. Dopamine, another MAO substrate which is increased in patients with carcinoid syndrome, also increased superoxide levels in heart valves, and this effect was attenuated by clorgyline. Apocynin did not prevent increases in O2.- during serotonin treatment. Addition of serotonin to recombinant human MAO-A generated superoxide, and this effect was prevented by an MAO inhibitor. In conclusion, I have demonstrated that ACE2 deficiency impairs vasomotor function in cerebral arteries from adult mice and augments endothelial dysfunction during aging. Oxidative stress plays a critical role in… Advisors/Committee Members: Heistad, Donald D. (supervisor).

Subjects/Keywords: Angiotensin Converting Enzyme Type 2; Angiotensin II; Cerebral Circulation; Heart Valves; Oxidative Stress; Pharmacology

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Pena Silva, R. A. (2012). Cardiovascular oxidative stress: recent findings on ACE2 And MAO. (Doctoral Dissertation). University of Iowa. Retrieved from https://ir.uiowa.edu/etd/3366

Chicago Manual of Style (16^th Edition):

Pena Silva, Ricardo Alfonso. “Cardiovascular oxidative stress: recent findings on ACE2 And MAO.” 2012. Doctoral Dissertation, University of Iowa. Accessed March 03, 2021. https://ir.uiowa.edu/etd/3366.

MLA Handbook (7^th Edition):

Pena Silva, Ricardo Alfonso. “Cardiovascular oxidative stress: recent findings on ACE2 And MAO.” 2012. Web. 03 Mar 2021.

Vancouver:

Pena Silva RA. Cardiovascular oxidative stress: recent findings on ACE2 And MAO. [Internet] [Doctoral dissertation]. University of Iowa; 2012. [cited 2021 Mar 03]. Available from: https://ir.uiowa.edu/etd/3366.

Council of Science Editors:

Pena Silva RA. Cardiovascular oxidative stress: recent findings on ACE2 And MAO. [Doctoral Dissertation]. University of Iowa; 2012. Available from: https://ir.uiowa.edu/etd/3366

University of Melbourne

22. CHEN, DAIAN. The role of angiotensin receptors in the brainstem in the regulation of sympathetic vasomotor activity.

Degree: 2011, University of Melbourne

URL: http://hdl.handle.net/11343/36131

► Cardiovascular diseases remain the leading cause of morbidity and mortality within Australian society and worldwide. Hypertension is a major contributing factor to the development of… (more)

▼ Cardiovascular diseases remain the leading cause of morbidity and mortality within Australian society and worldwide. Hypertension is a major contributing factor to the development of many cardiovascular diseases. One proposed cause of hypertension is the dysfuction of the renin-angiotensin system (RAS). The RAS plays a critical role in cardiovascular homeostasis by regulating blood pressure (BP) and fluid electrolyte balance. Due to this close relationship between the RAS and the pathogenesis of cardiovascular diseases, the studies outlined in this thesis attempt to further understand the complexities behind the RAS within the brain and how angiotensin II (Ang II) regulates BP. This is done with the use of transgenic mice with targeted deletion of RAS components together with viral vectors designed to induce cell-specific transgene expression in the rostral ventrolateral medulla (RVLM) of the brainstem. In Chapter 3, I examined whether targeted deletion of the angiotensinogen gene (Agt) altered brain Ang II receptor density and responsiveness to Ang II. There was overall little change in the receptor distribution and density in most brain regions in mice deficient for Agt compared to wild-types. I observed a small increase in the density of AT1 receptors in the RVLM of the Agt knockout mice, yet there was a diminished response to exogenous Ang II microinjection in the RVLM. This suggests that global deletion of Agt does not affect the expression of brain Ang II receptors, and that signal transduction pathways may be altered in RVLM neurons of Agt knockout mice, resulting in attenuated cellular excitation. In Chapter 4, I examined the effect of restoration of the functionally important Ang AT1A receptor via viral delivery designed to target cell-specific transgenic expression. First, I demonstrated that the response to Ang II microinjection in the RVLM was totally abolished in mice deficient for the AT1A receptor. This means that the Ang II-mediated excitation of RVLM neurons in adult mice is dependent upon the AT1A receptor with little or no effect of type 1B or 2 receptors. Another key finding was that the expression of the AT1A receptor predominantly in C1 catecholamine neurons restores the response to Ang II in the AT1A receptor deficient mice, demonstrating that these neurons are sympatho-excitatory. Increased BP reactivity to emotional stress is considered a risk factor for the development of cardiovascular diseases. In Chapter 5, I examined the involvement of AT1A receptors in the C1 catecholamine neurons of the RVLM in the cardiovascular responses to aversive and positive stimuli in conscious mice. I demonstrated a direct role for endogenous brain angiotensin acting in the RVLM on C1 neurons in the response to aversive stressors. These results provide direct support for the involvement of C1 neurons in the RVLM in the pressor responses to aversive, but not positive stimuli. …

Subjects/Keywords: blood pressure; hypertension; physiology; angiotensin II; renin angiotensin system; transgenic mice; sympathetic nervous system

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

CHEN, D. (2011). The role of angiotensin receptors in the brainstem in the regulation of sympathetic vasomotor activity. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/36131

Chicago Manual of Style (16^th Edition):

CHEN, DAIAN. “The role of angiotensin receptors in the brainstem in the regulation of sympathetic vasomotor activity.” 2011. Doctoral Dissertation, University of Melbourne. Accessed March 03, 2021. http://hdl.handle.net/11343/36131.

MLA Handbook (7^th Edition):

CHEN, DAIAN. “The role of angiotensin receptors in the brainstem in the regulation of sympathetic vasomotor activity.” 2011. Web. 03 Mar 2021.

Vancouver:

CHEN D. The role of angiotensin receptors in the brainstem in the regulation of sympathetic vasomotor activity. [Internet] [Doctoral dissertation]. University of Melbourne; 2011. [cited 2021 Mar 03]. Available from: http://hdl.handle.net/11343/36131.

Council of Science Editors:

CHEN D. The role of angiotensin receptors in the brainstem in the regulation of sympathetic vasomotor activity. [Doctoral Dissertation]. University of Melbourne; 2011. Available from: http://hdl.handle.net/11343/36131

Johannes Gutenberg Universität Mainz

23. Kossmann, Sabine. Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie.

Degree: 2014, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2014/3801/

► Im Rahmen dieser Arbeit wurde die Rolle von myelomonozytären Zellen, IFN-gamma (Interferon gamma), MyD88 (myeloid differentiation factor 88) und zugrundeliegenden Signalwege in der Angiotensin II… (more)

▼ Im Rahmen dieser Arbeit wurde die Rolle von myelomonozytären Zellen, IFN-gamma (Interferon gamma), MyD88 (myeloid differentiation factor 88) und zugrundeliegenden Signalwege in der Angiotensin II (ATII)-induzierten vaskulären Inflammation, Dysfunktion und arteriellen Hypertonie untersucht. Wie bereits veröffentlichte Vordaten aus meiner Arbeitsgruppe zeigten, schützt die Depletion von Lysozym M (LysM)+ myelomonozytären Zellen (Diphteriatoxin-vermittelt in Mäusen, die transgen für den humanen Diphtheriatoxin-Rezeptor sind, LysMiDTR Mäuse) vor der ATII-induzierten vaskulären Dysfunktion und arterieller Hypertonie, und kann durch adoptiven Zelltransfer von Wildtyp Monozyten wiederhergestellt werden. In meiner Arbeit konnte ich zeigen, dass die Rekonstitution von Monozyten-depletierten LysMiDTR Mäusen mit Wildtyp Monozyten den Phänotyp der vaskulären Dysfunktion wiederherstellen kann, die Rekonstitution mit gp91phox-/y oder Agtr1-/- Monozyten jedoch nicht. Die Hypertonus-mediierenden Effekte dieser infiltrierenden Monozyten scheinen demnach von der intakten ATII und NADPH Oxidase Signalübertragung in diesen Zellen abhängig zu sein. Vermutlich ebenfalls für die Aktivierung der Monozyten funktionell wichtig sind IFN-gamma, produziert durch NK-Zellen, und der Transkriptionsfaktor T-bet (T-box expressed in T cells), exprimiert von NK-Zellen und Monozyten. IFN-gamma-/- Mäuse waren partiell geschützt vor der ATII-induzierten vaskulären Dysfunktion und charakterisiert durch reduzierte Level an Superoxid im Gefäß im Vergleich zu ATII-infundierten Wildtyp Mäusen. IFN-gamma-/- und T-bet defiziente Tbx21-/- Mäuse zeichneten sich ferner durch eine reduzierte ATII-mediierte Rekrutierung von NK1.1+ NK-Zellen, als ein Hautproduzent von IFN-gamma, sowie CD11b+GR-1low Interleukin-12 (IL-12) kompetenten Monozyten aus. Durch Depletions- und adoptive Transferexperimente konnte ich in dieser Arbeit NK-Zellen als essentielle Mitstreiter in der vaskulären Dysfunktion identifizieren und stellte fest, dass T-bet+LysM+ myelomonozytäre Zellen für die NK-Zellrekrutierung in die Gefäßwand und lokale IFN-gamma Produktion benötigt werden. Damit wurde erstmals NK-Zellen eine essentielle Rolle in der ATII-induzierten vaskulären Dysfunktion zugeschrieben. Außerdem wurde der T-bet-IFN-gamma Signalweg und die gegenseitige Monozyten-NK-Zellaktivierung als ein potentielles therapeutisches Ziel in kardiovaskulären Erkrankungen aufgedeckt. Des Weiteren identifizierte ich in meiner Arbeit MyD88 als ein zentrales Signalmolekül in der ATII-getriebenen Inflammation und vaskulären Gefäßschädigung. MyD88 Defizienz reduzierte den ATII-induzierten Anstieg des systolischen Blutdrucks und die endotheliale und glattmuskuläre vaskuläre Dysfunktion. Zusätzlich waren die vaskuläre Superoxid-Bildung sowie die Expressionslevel der NADPH Oxidase, der wichtigsten Quelle für oxidativem Stress im Gefäß, in ATII-infundierten MyD88-/- Mäusen im Vergleich zum Wildtyp reduziert. Mit Hilfe von durchflusszytometrischen Analysen deckte ich zudem auf, dass die ATII-induzierte…

Subjects/Keywords: Inflammation; arterielle Hypertonie; vaskuläre Dysfunktion; Angiotensin II; IFN-gamma; inflammation; arterial hypertension; vascular dysfunction; Angiotensin II; IFN-gamma; Life sciences

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Kossmann, S. (2014). Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2014/3801/

Chicago Manual of Style (16^th Edition):

Kossmann, Sabine. “Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie.” 2014. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed March 03, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2014/3801/.

MLA Handbook (7^th Edition):

Kossmann, Sabine. “Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie.” 2014. Web. 03 Mar 2021.

Vancouver:

Kossmann S. Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2014. [cited 2021 Mar 03]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2014/3801/.

Council of Science Editors:

Kossmann S. Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2014. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2014/3801/

Johannes Gutenberg Universität Mainz

24. Krimm, Daniela. Untersuchung der Rolle reaktiver Sauerstoffspezies und DNA-Schäden bei Hypertonie und Arteriosklerose.

Degree: 2014, Johannes Gutenberg Universität Mainz

URL: http://ubm.opus.hbz-nrw.de/volltexte/2014/3821/

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Angiotensin II induziert intrazellulär die Bildung reaktiver Sauerstoffspezies, welche DNA-Schäden erzeugen können. Um die Hypothese zu prüfen, dass durch Angiotensin II induzierte DNA-Schäden für die… (more)

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Angiotensin II induziert intrazellulär die Bildung reaktiver Sauerstoffspezies, welche DNA-Schäden erzeugen können. Um die Hypothese zu prüfen, dass durch Angiotensin II induzierte DNA-Schäden für die erhöhte Krebsinzidenz hypertensiver Menschen verantwortlich sind, wurde eine vierwöchige Behandlung von Mäusen mit Angiotensin II (0,6 μg/kg/min) durchgeführt. Mit der Alkalischen Elution wurden in Zellen aus verschiedenen Organen der Mäuse die Menge an DNA-Einzelstrangbrüchen und oxidativen DNA-Modifikationen bestimmt. In der Niere wurde außerdem mit dem BigBlue® Mutations-Assay die Entstehung von Mutationen analysiert. In keinem der analysierten Organe konnte eine Erhöhung der DNA-Schäden oder eine Erhöhung der Mutationsfrequenzen durch die Angiotensin II-Behandlung nachgewiesen werden. Die durchgeführten Untersuchungen geben somit keinen Hinweis auf eine DNA-schädigende und mutagene Wirkung von Angiotensin II.rnBei der Entstehung und dem Krankheitsverlauf von Arteriosklerose spielen reaktive Sauerstoffspezies ebenfalls eine noch nicht genau geklärte Rolle. Um zu ermitteln, ob oxidative DNA-Schäden die Entstehung der Arteriosklerose begünstigen, wurde die Endothelfunktion von Wildtyp- und reparaturdefizienten Ogg1-/ – Mäusen verglichen. Entgegen der Vermutung, dass oxidative DNA-Modifikationen die Endothelfunktion verschlechtern, zeigen die Untersuchungen, dass Ogg1-/ – Mäuse, die höhere Spiegel an oxidativen DNA-Modifikationen in ihrem Genom haben, eine signifikant bessere Endothelfunktion besitzen als Wildtyptiere. Dieser Befund weist auf eine neuartige, von der DNA-Reparatur unabhängige Funktion von OGG1 hin.rn

Angiotensin II intracellularly stimulates the generation of reactive oxygen species, which can induce DNA damage. In order to test the hypothesis that DNA damage generated by angiotensin II is responsible for the elevated cancer incidence of hypertensive people, we treated mice for 4 weeks with angiotensin II (0.6 μg/kg/min) and quantified the frequencies of oxidative DNA modifications (using an Alkaline Elution assay) and mutations in kidneys (using a BigBlue® mutation assay). No increase of DNA damage or mutation frequencies following angiotensin II treatment were detected in any of the organs analyzed. The results do not support the assumption that angiotensin II is genotoxic in vivo.rnThe role of reactive oxygen species in the etiology of atherosclerosis has not yet been fully established. To determine whether oxidative DNA damage promotes atherosclerosis, we compared the endothelial function of wild-type and repair deficient Ogg1-/ – mice. Contrary to the expectation that oxidative DNA damage impairs the endothelial function, the data shows that Ogg1-/ – mice (with higher levels of oxidative DNA modifications in their genome) have a better endothelial function than wild-type mice. These results indicate a new, from DNA repair independent function of OGG1.rn

Subjects/Keywords: DNA-Schäden; reaktive Sauerstoffspezies; Angiotensin II; Hypertonie; Arteriosklerose; DNA damage; reactive oxygen species; angiotensin ii; hypertension; atherosclerosis; Natural sciences and mathematics

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Krimm, D. (2014). Untersuchung der Rolle reaktiver Sauerstoffspezies und DNA-Schäden bei Hypertonie und Arteriosklerose. (Doctoral Dissertation). Johannes Gutenberg Universität Mainz. Retrieved from http://ubm.opus.hbz-nrw.de/volltexte/2014/3821/

Chicago Manual of Style (16^th Edition):

Krimm, Daniela. “Untersuchung der Rolle reaktiver Sauerstoffspezies und DNA-Schäden bei Hypertonie und Arteriosklerose.” 2014. Doctoral Dissertation, Johannes Gutenberg Universität Mainz. Accessed March 03, 2021. http://ubm.opus.hbz-nrw.de/volltexte/2014/3821/.

MLA Handbook (7^th Edition):

Krimm, Daniela. “Untersuchung der Rolle reaktiver Sauerstoffspezies und DNA-Schäden bei Hypertonie und Arteriosklerose.” 2014. Web. 03 Mar 2021.

Vancouver:

Krimm D. Untersuchung der Rolle reaktiver Sauerstoffspezies und DNA-Schäden bei Hypertonie und Arteriosklerose. [Internet] [Doctoral dissertation]. Johannes Gutenberg Universität Mainz; 2014. [cited 2021 Mar 03]. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2014/3821/.

Council of Science Editors:

Krimm D. Untersuchung der Rolle reaktiver Sauerstoffspezies und DNA-Schäden bei Hypertonie und Arteriosklerose. [Doctoral Dissertation]. Johannes Gutenberg Universität Mainz; 2014. Available from: http://ubm.opus.hbz-nrw.de/volltexte/2014/3821/

25. Viegas, Katia Aparecida da Silva. Ação da angiotensina II no remodelamento da matriz extracelular perivascular em camundongos.

Degree: PhD, Ciências Morfofuncionais, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42131/tde-29012013-082719/ ;

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Neste estudo avaliou-se a ação da Angiotensina II (Ang II) e do bloqueio dos seus receptores AT1 e AT2 no remodelamento da matriz extracelular (MEC)… (more)

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Neste estudo avaliou-se a ação da Angiotensina II (Ang II) e do bloqueio dos seus receptores AT1 e AT2 no remodelamento da matriz extracelular (MEC) e traçamos o perfil da sinalização intracelular envolvida no processo. O estudo foi feito in vivo em camundongos isogênicos C57Bl/6J submetidos a tratamento durante 7 e 14 dias com doses subpressoras de Ang II, bloqueador do receptor AT1 (Losartan) e uma combinação destes. Os animais foram sacrificados e procedeu-se a coleta de tecidos de artérias (aorta, carótida e femoral), coração, rins e pulmão para análise da síntese e degradação de componentes da MEC. Foram feitas avaliações hemodinâmicas, morfológicas em microscopia de luz, morfométricas, imunohistoquímicas para os componentes da matriz extracelular: colágeno (tipos I, III, IV e VI), fibronectina, tenascina-C, elastina, metaloproteinases (tipos 2 e 9), e quantificação de algumas proteínas ligadas à sinalização intracelular da via das Proteínas quinases ativadas por mitógenos (MAPK - Mitogen-activated protein kinases) usando-se Western Blotting.

In this study we evaluated the action of Angiotensin II (Ang II) and the blockade of AT1 and AT2 receptors in the remodeling of extracellular matrix (ECM) and outlines the process involved in intracellular signaling. The study was done in vivo in C57Bl/6J inbred mice undergoing treatment for 7 and 14 days subpressor doses of Ang II, AT1 receptor blocker (Losartan) and a combination thereof. The animals were sacrificed and proceeded to collect tissues of arteries (aorta, carotid and femoral arteries), heart, kidneys and lungs for analysis of the synthesis and degradation of ECM components. We assessed hemodynamic, morphological light microscopy, morphometry, immunohistochemistry for extracellular matrix components: collagen (types I, III, IV and VI), fibronectin, tenascin-C, elastin, metalloproteinases (types 2 and 9) and quantification of some proteins related to intracellular signaling pathways of the mitogen-activated protein kinase (MAPK) using Western Blotting.

Advisors/Committee Members: Lacchini, Silvia.

Subjects/Keywords: Angiotensin II; Angiotensin receptors; Angiotensina II; Blood vessels; Camundongos; Mice; Receptores de angiotensina; Vasos sanguíneos; Western blotting; Western blotting

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Viegas, K. A. d. S. (2012). Ação da angiotensina II no remodelamento da matriz extracelular perivascular em camundongos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42131/tde-29012013-082719/ ;

Chicago Manual of Style (16^th Edition):

Viegas, Katia Aparecida da Silva. “Ação da angiotensina II no remodelamento da matriz extracelular perivascular em camundongos.” 2012. Doctoral Dissertation, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-29012013-082719/ ;.

MLA Handbook (7^th Edition):

Viegas, Katia Aparecida da Silva. “Ação da angiotensina II no remodelamento da matriz extracelular perivascular em camundongos.” 2012. Web. 03 Mar 2021.

Vancouver:

Viegas KAdS. Ação da angiotensina II no remodelamento da matriz extracelular perivascular em camundongos. [Internet] [Doctoral dissertation]. University of São Paulo; 2012. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42131/tde-29012013-082719/ ;.

Council of Science Editors:

Viegas KAdS. Ação da angiotensina II no remodelamento da matriz extracelular perivascular em camundongos. [Doctoral Dissertation]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/42/42131/tde-29012013-082719/ ;

26. Loiola, Rodrigo Azevedo. Venoconstrição induzida por angiotensina II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2.

Degree: Mestrado, Farmacologia, 2007, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-28012008-103638/ ;

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Neste estudo, avaliamos e caracterizamos o efeito de Ang II em leito venular mesentérico (LVM) e anéis de veia porta (AVP) de wistar e SHR.… (more)

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Neste estudo, avaliamos e caracterizamos o efeito de Ang II em leito venular mesentérico (LVM) e anéis de veia porta (AVP) de wistar e SHR. A reatividade vascular para Ang II foi estudada na presença e ausência de diferentes antagonistas para elucidar os mecanismos envolvidos na venoconstrição induzida por Ang II. Nossos resultados sugerem que a Ang II induz venoconstrição através da ativação de receptores AT1 e AT2 em Wistar e receptor AT1 em SHR. Essa venoconstrição parece ser contrabalanceada pelo receptor B2 em ambas as espécies. NO contribue para este efeito em wistar e metabólitos da COX em SHR. Há redução da venoconstrição induzida por Ang II em AVP de SHR que pode estar relacionado a redução da expressão protéica de receptores AT2. Esses resultados indicam diferentes mecanismos de regulação do tônus venoso de ratos wistar e SHR em resposta a Ang II que podem ter relevância no controle do retorno venoso e débito cardíaco.

In this study we have evaluated and characterized the effect of Ang II in the isolated perfused mesenteric venular bed (MVB) and portal vein rings (PVR) of SHR and wistar rats. Vascular reactivity to Ang II was studied in the absence and presence of different antagonists to elucidate the mechanisms involved in Ang II-induced venoconstriction. Our results suggest that Ang II induces venoconstriction by activation of AT1 and AT2 receptors in wistar and AT1 receptor in SHR. These venoconstriction seems to be counterbalanced by B2 receptor in both species. NO might contribute to this effect in wistar and COX metabolites in SHR. There is a decrease in Ang II induced venoconstriction in PVR of SHR that might be related to the decrease of protein expression of AT2 receptor. These results indicate different mechanisms of regulation of venous tonus of the SHR and wistar rats induced by Ang II that can be relevant in the control of the venous return and cardiac output.

Advisors/Committee Members: Carvalho, Maria Helena Catelli de.

Subjects/Keywords: Angiotensin II; Angiotensina II; Hipertensão; Hypertension; Renin angiotensin system; Sistema renina angiotensina; Sistema venoso.; Venous system.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Loiola, R. A. (2007). Venoconstrição induzida por angiotensina II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2. (Masters Thesis). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42136/tde-28012008-103638/ ;

Chicago Manual of Style (16^th Edition):

Loiola, Rodrigo Azevedo. “Venoconstrição induzida por angiotensina II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2.” 2007. Masters Thesis, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-28012008-103638/ ;.

MLA Handbook (7^th Edition):

Loiola, Rodrigo Azevedo. “Venoconstrição induzida por angiotensina II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2.” 2007. Web. 03 Mar 2021.

Vancouver:

Loiola RA. Venoconstrição induzida por angiotensina II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2. [Internet] [Masters thesis]. University of São Paulo; 2007. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-28012008-103638/ ;.

Council of Science Editors:

Loiola RA. Venoconstrição induzida por angiotensina II em ratos normotensos e hipertensos: estudo de mecanismos de ação, localização e expressão de receptores AT1 e AT2. [Masters Thesis]. University of São Paulo; 2007. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-28012008-103638/ ;

Freie Universität Berlin

27. Danyel, Leon Alexander. In vitro screening for intrinsic activity of potential AT2R–agonists in differentiated THP-1-macrophages.

Degree: 2018, Freie Universität Berlin

URL: http://dx.doi.org/10.17169/refubium-8637

► Accumulating evidence suggests tissue-protective properties of pharmacological AT2R-stimulation in various animal models of cerebral and cerebrovascular disease. Further investigation of the neuroprotective properties of pharmacological… (more)

▼ Accumulating evidence suggests tissue-protective properties of pharmacological AT2R-stimulation in various animal models of cerebral and cerebrovascular disease. Further investigation of the neuroprotective properties of pharmacological AT2R-stimulation is hindered, because common AT2R-agonists like CGP42112 and the non-peptide agonist Compound 21 cannot penetrate the blood-brain barrier. Therefore, a new generation of blood-brain barrier- penetrating AT2R-agonists is being developed. New substances, designed through chemical alteration of established molecules, need to be reevaluated for AT2R–affinity and intrinsic activity. Common assays available, e. g. the Neurite-Outgrowth-assay are considered to be unreliable on the grounds of subjective analysis and imprecise quantification of results. Therefore, this project aimed at establishing a reliable and robust in vitro screening of potential AT2R–agonists for intrinsic activity at the AT2R based on determining interleukin 6 (IL-6) mRNA expression in THP-1-macrophages. AT2R- protein expression in THP-1-monocytes was compared with AT2R-protein expression in PMA-differentiated THP-1-macrophages using Western-Blot analysis. Effects of LPS- (50 ng/ml) and Compound 21- (1 µM) incubation on AT2R-protein-expression in THP-1-macrophages were evaluated. THP-1-macrophages were incubated with LPS (50 ng/ml), co-treated with the novel agents JS5090, L162-389 and VR0008 (1 µM each) for 6 hours and IL-6-mRNA expression determined by qPCR. AT2R-agonist Compound 21 was used for reference. AT2R- agonism was postulated if the substance in question attenuated the increase of LPS-induced IL-6-mRNA expression. The AT2R -antagonist PD123319 (10 µM) was used to confirm AT2R -specificity of observed effects. PMA-induced differentiation of THP-1 monocytes to macrophages increased expression of the AT2R-receptor-protein tenfold in Western Blot analysis (single experiment, p = 0,0002). Incubation with LPS and Compound 21 each significantly decreased AT2R-receptor-protein-expression (single experiment, p = 0,0001 and p = 0,0008 respectively). Treatment of THP-1 macrophages with JS5090, L162-389, VR0008, or Compound 21 did not result in consistent, significant effects on LPS- induced IL-6-mRNA-expression. JS5090, L162-389 and VR0008 could not be verified as AT2R-receptor agonists. Since the established AT2R-Agonist Compound 21 also did not elicit consistent effects on LPS-induced IL-6-mRNA- expression in our assay, we conclude that the tested assay was of limited validity probably due to unpredictable effects of PMA-induced differentiation and LPS-incubation of THP-1-macrophages. Future protocols should be optimized to achieve controlled and inter-experimentally consistent PMA-induced differentiation of THP-1-monocytes. In conclusion, the current IL-6-THP-1-assay has to be regarded as not suitable for the screening of potential AT2R-receptor agonists. Advisors/Committee Members: m (gender), N. N. (firstReferee), N. N. (furtherReferee).

Subjects/Keywords: Angiotensin II Type 2 receptor; THP-1; Angiotensin II; Compound 21; PD123319; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Danyel, L. A. (2018). In vitro screening for intrinsic activity of potential AT2R–agonists in differentiated THP-1-macrophages. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-8637

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Danyel, Leon Alexander. “In vitro screening for intrinsic activity of potential AT2R–agonists in differentiated THP-1-macrophages.” 2018. Thesis, Freie Universität Berlin. Accessed March 03, 2021. http://dx.doi.org/10.17169/refubium-8637.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Danyel, Leon Alexander. “In vitro screening for intrinsic activity of potential AT2R–agonists in differentiated THP-1-macrophages.” 2018. Web. 03 Mar 2021.

Vancouver:

Danyel LA. In vitro screening for intrinsic activity of potential AT2R–agonists in differentiated THP-1-macrophages. [Internet] [Thesis]. Freie Universität Berlin; 2018. [cited 2021 Mar 03]. Available from: http://dx.doi.org/10.17169/refubium-8637.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Danyel LA. In vitro screening for intrinsic activity of potential AT2R–agonists in differentiated THP-1-macrophages. [Thesis]. Freie Universität Berlin; 2018. Available from: http://dx.doi.org/10.17169/refubium-8637

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

28. Pedro Henrique SÃ Costa. ModulaÃÃo da via das guanilinas pelo enalapril em ratos submetidos Ã nefrectomia 5/6.

Degree: Master, 2015, Universidade Federal do Ceará

URL: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13912 ;

► A doenÃa renal crÃnica (DRC) Ã caracterizada pela perda normalmente lenta, progressiva e irreversÃvel da funÃÃo renal. Sugere-se que, nesta patologia, a resposta natriurÃtica do… (more)

▼ A doenÃa renal crÃnica (DRC) Ã caracterizada pela perda normalmente lenta, progressiva e irreversÃvel da funÃÃo renal. Sugere-se que, nesta patologia, a resposta natriurÃtica do organismo Ã ingestÃo de sal e a expansÃo de volume encontra-se reduzida em consequÃncia da lesÃo dos nÃfrons. Nesse contexto, mostram-se necessÃrios estudos que estabeleÃam uma relaÃÃo entre a DRC e a regulaÃÃo de peptÃdeos natriurÃticos, como guanilina (Gn), uroguanilina (UGn) e peptÃdeo natriurÃtico atrial (PNA), e o efeito da angiotensina II (AngII) sobre a regulaÃÃo destes peptÃdeos. Assim, buscou-se avaliar uma possÃvel modulaÃÃo da via das guanilinas pelo enalapril no modelo de nefrectomia 5/6 (nx5/6). Utilizou-se ratos Wistar, machos, com peso entre 250-300g. Os animais foram divididos em 4 grupos (n=8): grupos controle sem tratamento ou tratado com enalapril (10mg/kg v.o.) (SHAM e SHAM+E) e grupos submetidos Ã nx 5/6 sem tratamento ou tratado com enalapril (10 mg/kg v.o.) (Nx e Nx+E). Ao final da 10Â semana apÃs a cirurgia, foram determinados alguns marcadores de funÃÃo renal. As amostras de rim foram encaminhadas para anÃlise histolÃgica e avaliaÃÃo expressÃo de RNAm para Gn, UGn, PNA e dos receptores da guanilato ciclase de membrana, GC-A e GC-C e do receptor de clearence (NPR-C). No intestino, determinou-se a expressÃo de RNAm para Gn, UGn e G-C. Nx apresentou os nÃveis sÃricos de creatinina (Nx= 1.28 Â 0.07; SHAM= 0.67 Â 0.02 mg/dL), urÃia (Nx=108.0 Â 5.57; SHAM=96.83 Â 4.08 mg/dL), proteinÃria (Nx=129.10 Â 13.87 SHAM=96.83 Â 4.07; mg/24hrs) e FENa+ (Nx=3.552 Â 0.56; SHAM=1.43 Â 0.16) aumentados, e a TFG (Nx=0.44 Â 0.10 Â 0.04; SHAM=0.97 Â 0.07 mL/min) diminuÃda. Nx+E, quando comparado a Nx, apresentou nÃveis reduzidos de creatinina (Nx+E= 0.97 Â 0.08; Nx=1.28 Â 0.07 mg/dL), de proteinÃria (Nx+E=31.94 Â 6.46 Nx= 129.10 Â 13.87 mg/24hrs) e da FENa+ (Nx+E= 2.02 Â 0.28; Nx=3.55 Â 0.56), alÃm elevar a TFG (Nx+E=0.70 Â 0.08; Nx=0.44 Â 0.10 mL/min). Nx apresentou aumento da expressÃo gÃnica intra-renal de Gn (Nx=13.92 Â 5.13; SHAM=1.08 Â 0.20), UGn (Nx=12.77 Â 7.00; SHAM=1.04 Â 0.13), GC-A (Nx=5.91 Â 1.36; SHAM=1.06 Â 0.17) e NPR-C (Nx=7.835 Â 1.72; SHAM=1.15 Â 0.27), e Nx+E teve genes reduzidos para UGn (Nx+E=0.10 Â 0.03; Nx=1.75 Â 0.96), GC-A (Nx+E=0.031 Â 0.01; Nx=1.18 Â 0.27) e NPR-C (Nx+E=0.03 Â 0.01; Nx=1.08 Â 0.24) quando comparados a Nx. No intestino, houve uma reduÃÃo da transcriÃÃo de GC-C (Nx=0,22Â0,04; SHAM=1.12 Â 0.22) em Nx, e o enalapril aumentou os nÃveis de expressÃo deste gene (Nx+E=3.94 Â 0.57; Nx=1.15 Â 0.22). Em conjunto, estes dados sugerem uma hiperativaÃÃo na via das guanilinas na DRC, alÃm de modulaÃÃo dessa classe de peptÃdeos por parte da AngII. Advisors/Committee Members: Helena Serra Azul Monteiro, Ana Durce Oliveira da PaixÃo, LucÃlia Maria Abreu Lessa.

Subjects/Keywords: ZOOTECNIA; InsuficiÃncia Renal CrÃnica; Enalapril; Angiotensina II; Natriurese; Chronic kidney disease; Enalapril; Angiotensin II; Natriuresis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Costa, P. H. S. (2015). ModulaÃÃo da via das guanilinas pelo enalapril em ratos submetidos Ã nefrectomia 5/6. (Masters Thesis). Universidade Federal do Ceará. Retrieved from http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13912 ;

Chicago Manual of Style (16^th Edition):

Costa, Pedro Henrique SÃ. “ModulaÃÃo da via das guanilinas pelo enalapril em ratos submetidos Ã nefrectomia 5/6.” 2015. Masters Thesis, Universidade Federal do Ceará. Accessed March 03, 2021. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13912 ;.

MLA Handbook (7^th Edition):

Costa, Pedro Henrique SÃ. “ModulaÃÃo da via das guanilinas pelo enalapril em ratos submetidos Ã nefrectomia 5/6.” 2015. Web. 03 Mar 2021.

Vancouver:

Costa PHS. ModulaÃÃo da via das guanilinas pelo enalapril em ratos submetidos Ã nefrectomia 5/6. [Internet] [Masters thesis]. Universidade Federal do Ceará 2015. [cited 2021 Mar 03]. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13912 ;.

Council of Science Editors:

Costa PHS. ModulaÃÃo da via das guanilinas pelo enalapril em ratos submetidos Ã nefrectomia 5/6. [Masters Thesis]. Universidade Federal do Ceará 2015. Available from: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=13912 ;

29. Felix, Jorge Vinicius Cestari. Estudo das vias intracelulares de sinalização da insulina e da angiotensina-II no hipotálamo de ratas grávidas e lactantes.

Degree: PhD, Fisiologia Humana, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42137/tde-29012013-091434/ ;

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A gestação é um período em que a fêmea é transitoriamente submetida a uma série de alterações em todo o organismo, resultando num quadro semelhante… (more)

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A gestação é um período em que a fêmea é transitoriamente submetida a uma série de alterações em todo o organismo, resultando num quadro semelhante à síndrome metabólica, mas que são cuidadosamente reguladas de modo a fornecer o suprimento adequado de substratos para a mãe e para o feto. A gravidez caracteriza-se como modelo fisiológico e temporalmente definido de resistência à insulina. Já durante a lactação, observa-se hipersensibilidade sistêmica à ação da insulina. A ativação de vias de sinalização da insulina no cérebro, em particular no núcleo arqueado do hipotálamo (ARC), tem importante papel na regulação da homeostasia glicêmica. Já está bem estabelecido que a Ang-II é capaz de induzir a fosforilação em serina do IR, do IRS e da subunidade regulatória p85 da PI3K. No entanto, ainda não foi esclarecido se ocorrem alterações na via de sinalização da insulina em áreas do sistema nervoso central (SNC) responsáveis pelo controle da homeostasia glicêmica, como é o caso do ARC, do núcleo hipotalâmico ventromedial (VMH) e do núcleo paraventricular (PVN) durante a gestação, que poderia contribuir para o quadro de resistência à insulina nesta situação. O objetivo deste estudo foi avaliar a expressão das proteínas de sinalização intracelular da insulina IRS1-2, PI3K (p85α, p55α, p50α), AKT, p-Ser473 AKT e dos receptores IR, e AT1a no hipotálamo total e no ARC, VMH e PVN na gravidez e na lactação. Investigou-se também o possível cross-talk da via de sinalização da insulina e da Angiotensina-II (Ang-II) no hipotálamo. Observou-se a redução da expressão do IRS-2, da AKT e da p-Ser473 AKT, concomitante com o aumento da expressão das subunidades regulatórias p85α, p55α, p50α da PI3K e do receptor AT1a no hipotálamo na gravidez. No ARC, VMH e PVN observou-se co-localização da p85α e do receptor AT1a, bem como aumento da expressão de ambos nessas regiões, nas ratas grávidas. O tratamento crônico com antagonista AT1 (losartan) produziu, nas grávidas redução significativa da expressão deste receptor, sem causar alteração na expressão da p85α. A disfunção das vias da Ang-II e da insulina em graus variados pode levar a duas condições patológicas de alta prevalência e que muitas vezes são concomitantes: diabetes mellitus e hipertensão arterial. A melhor compreensão das alterações hipotalâmicas nas vias de sinalização da insulina e da Ang-II, bem como a caracterização molecular dessa interação, tanto nas situações fisiológicas (por exemplo na gravidez) como nas situações patológicas, poderá revelar alvos para futuras intervenções terapêuticas para diversas condições clínicas como a obesidade, o diabetes, a hipertensão arterial, a pré-eclâmpsia/eclâmpsia, etc...

Pregnancy is a period in which the female is temporarily exposed to a series of changes throughout the body, resulting in a condition similar to the metabolic…

Advisors/Committee Members: Silva, Silvana Auxiliadora Bordin da.

Subjects/Keywords: Angiotensin II; Angiotensina II; Gravidez; Hipotálamo; Hypothalamus; Infants; Insulin; Insulina; Lactentes; Mice; Pregnancy; Ratos

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Felix, J. V. C. (2012). Estudo das vias intracelulares de sinalização da insulina e da angiotensina-II no hipotálamo de ratas grávidas e lactantes. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42137/tde-29012013-091434/ ;

Chicago Manual of Style (16^th Edition):

Felix, Jorge Vinicius Cestari. “Estudo das vias intracelulares de sinalização da insulina e da angiotensina-II no hipotálamo de ratas grávidas e lactantes.” 2012. Doctoral Dissertation, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-29012013-091434/ ;.

MLA Handbook (7^th Edition):

Felix, Jorge Vinicius Cestari. “Estudo das vias intracelulares de sinalização da insulina e da angiotensina-II no hipotálamo de ratas grávidas e lactantes.” 2012. Web. 03 Mar 2021.

Vancouver:

Felix JVC. Estudo das vias intracelulares de sinalização da insulina e da angiotensina-II no hipotálamo de ratas grávidas e lactantes. [Internet] [Doctoral dissertation]. University of São Paulo; 2012. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42137/tde-29012013-091434/ ;.

Council of Science Editors:

Felix JVC. Estudo das vias intracelulares de sinalização da insulina e da angiotensina-II no hipotálamo de ratas grávidas e lactantes. [Doctoral Dissertation]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/42/42137/tde-29012013-091434/ ;

30. Silva, Sergio Marinho da. Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos.

Degree: PhD, Fisiologia Geral, 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16012015-112025/ ;

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O controle neural da pressão arterial é essencial para a manutenção da homeostase do organismo. Este controle é realizado principalmente por núcleos bulbares e hipotalâmicos.… (more)

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O controle neural da pressão arterial é essencial para a manutenção da homeostase do organismo. Este controle é realizado principalmente por núcleos bulbares e hipotalâmicos. Um dos principais sistemas de neurotransmissão envolvidos no controle da pressão arterial é o catecolaminérgico. Células noradrenérgicas e adrenérgicas estão presentes em todos os centros bulbares reguladores da pressão arterial, enquanto seus receptores, principalmente o receptor α2 adrenérgico (α2r), estão presentes nas mesmas regiões além de estarem presentes também nos núcleos hipotalâmicos. Estes receptores, quando ativados nestes núcleos, geram respostas cardiovasculares e atuam em conjunto com outros sistemas de neurotransmissão neste controle. Dentre estes sistemas de neurotransmissão, merecem destaque os sistemas angiotensinérgico e glutamatérgico, não apenas por estarem presentes nestes núcleos, mas também por atuarem no controle da pressão arterial. Contudo, pouco se sabe sobre como o sistema catecolaminérgico interage com estes sistemas. Desta forma, estudamos neste projeto a influência do sistema glutamatérgico e angiotensinérgico sobre o sistema catecolaminérgico no bulbo de ratos. Através de culturas de células bulbares, demonstramos que a ativação de receptores glutamatérgicos do tipo NMDA é capaz de elevar os níveis proteicos do α2R e que os receptores ionotrópicos do tipo não-NMDA precisam estar desbloqueados para tal. Em ratos adultos, microinjeções repetidas inibem a resposta bradicárdica induzida pela ativação dos α2rR no NTS. Contudo, o knockdown dos receptores AT1 de angiotensina restaura a resposta bradicárdica. A partir destes resultados, foi demonstrado que o sistema glutamatérgico é capaz de modular o sistema catecolaminérgico, enquanto o knockdown do receptor AT1 de angiotensina no NTS acentua a resposta bradicárdica dos α2R do NTS. Estes resultados sugerem que os sistemas de neurotransmissão bulbares interagem de diferentes formas e a compreensão deste controle pode vir a ser de grande valia para a compreensão de como se dá o controle da pressão arterial pelo sistema nervoso

The neural control of blood pressure is essential for the maintenance of the homeostasis of the organism. This control is performed mainly by nuclei in the medulla oblongata and in the hypothalamus. One of the main neurotransmitter system involved in this control is the catecholaminergic. Noradrenergic and adrenergic cells are present in all medullary nuclei involved in the arterial pressure regulation, while its receptors, especially the α2 adrenoceptor, are present in the same region plus hypothalamic nuclei. These receptors, upon activation in these nuclei, generate cardiovascular response, and act with other neurotransmission systems in this control. Among these systems, the glutamatergic and angiotensinergic deserve attention not only for also being present in the same nuclei, but for also acting in the control of the arterial pressure. Both angiotensinergic and glutamatergic systems interact with the…

Advisors/Committee Members: Chadi, Debora Rejane Fior.

Subjects/Keywords: α 2 adrenoceptor; Angiotensin II; Angiotensina II; Glutamate; Glutamato; Receptor α 2 adrenérgico

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Silva, S. M. d. (2014). Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16012015-112025/ ;

Chicago Manual of Style (16^th Edition):

Silva, Sergio Marinho da. “Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos.” 2014. Doctoral Dissertation, University of São Paulo. Accessed March 03, 2021. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16012015-112025/ ;.

MLA Handbook (7^th Edition):

Silva, Sergio Marinho da. “Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos.” 2014. Web. 03 Mar 2021.

Vancouver:

Silva SMd. Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2021 Mar 03]. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16012015-112025/ ;.

Council of Science Editors:

Silva SMd. Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/41/41135/tde-16012015-112025/ ;

Open Access Theses and Dissertations