subject:(Angiotensin II physiology mesh )

University of Florida

1. Kalberg, Christopher John, 1961-. Mechanisms of neuronal angiotensin II receptor regulation.

Degree: 1989, University of Florida

URL: https://ufdc.ufl.edu/AA00061932

Subjects/Keywords: Angiotensin II – physiology ( mesh ); Receptors, Angiotensin ( mesh ); Physiology thesis Ph.D ( mesh )

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

APA (6^th Edition):

Kalberg, Christopher John, 1. (1989). Mechanisms of neuronal angiotensin II receptor regulation. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00061932

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):

Kalberg, Christopher John, 1961-. “Mechanisms of neuronal angiotensin II receptor regulation.” 1989. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00061932.

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

MLA Handbook (7^th Edition):

Kalberg, Christopher John, 1961-. “Mechanisms of neuronal angiotensin II receptor regulation.” 1989. Web. 19 Jan 2021.

Vancouver:

Kalberg, Christopher John 1. Mechanisms of neuronal angiotensin II receptor regulation. [Internet] [Thesis]. University of Florida; 1989. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00061932.

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

Council of Science Editors:

Kalberg, Christopher John 1. Mechanisms of neuronal angiotensin II receptor regulation. [Thesis]. University of Florida; 1989. Available from: https://ufdc.ufl.edu/AA00061932

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

University of Florida

2. Rydzewski, Bartosz, 1967-. Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system.

Degree: 1992, University of Florida

URL: https://ufdc.ufl.edu/AA00066134

Subjects/Keywords: Research ( mesh ); Angiotensin II – physiology ( mesh ); Angiotensin II – pharmacology ( mesh ); Protease Inhibitors – metabolism ( mesh ); Plasminogen Activator Inhibitor 1 – metabolism ( mesh ); RNA, Messenger – metabolism ( mesh ); Central Nervous System – physiology ( mesh ); Gene Expression Regulation ( mesh ); Rats, Inbred WKY ( mesh ); Astrocytes ( mesh ); Brain – physiology ( mesh ); Department of Physiology thesis Ph.D ( mesh )

Record Details Similar Records Cite « Share

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

APA (6^th Edition):

Rydzewski, Bartosz, 1. (1992). Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00066134

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):

Rydzewski, Bartosz, 1967-. “Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system.” 1992. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00066134.

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

MLA Handbook (7^th Edition):

Rydzewski, Bartosz, 1967-. “Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system.” 1992. Web. 19 Jan 2021.

Vancouver:

Rydzewski, Bartosz 1. Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system. [Internet] [Thesis]. University of Florida; 1992. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00066134.

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

Council of Science Editors:

Rydzewski, Bartosz 1. Angiotensin II regulates the expression of extracellular protease inhibitors in the central nervous system. [Thesis]. University of Florida; 1992. Available from: https://ufdc.ufl.edu/AA00066134

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

University of Melbourne

3. 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 January 19, 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. 19 Jan 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 Jan 19]. 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

Tulane University

4. 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 January 19, 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. 19 Jan 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 Jan 19]. 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 Florida

5. Trolliet Baumann, Maria Rosa, 1960-. Hormonal and salt regulation of peripheral and brain renin-angiotensin system separated by nephrectomy.

Degree: 1993, University of Florida

URL: https://ufdc.ufl.edu/AA00066672

Subjects/Keywords: Research ( mesh ); Nephrectomy ( mesh ); Angiotensin II ( mesh ); Angiotensinogen ( mesh ); Renin-Angiotensin System ( mesh ); Plasma – chemistry ( mesh ); Brain Chemistry ( mesh ); Dialysis – methods ( mesh ); Water-Electrolyte Balance ( mesh ); Electrolytes ( mesh ); Hormones ( mesh ); Rats ( mesh ); Department of Physiology thesis Ph.D ( mesh )

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

APA (6^th Edition):

Trolliet Baumann, Maria Rosa, 1. (1993). Hormonal and salt regulation of peripheral and brain renin-angiotensin system separated by nephrectomy. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00066672

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):

Trolliet Baumann, Maria Rosa, 1960-. “Hormonal and salt regulation of peripheral and brain renin-angiotensin system separated by nephrectomy.” 1993. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00066672.

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

MLA Handbook (7^th Edition):

Trolliet Baumann, Maria Rosa, 1960-. “Hormonal and salt regulation of peripheral and brain renin-angiotensin system separated by nephrectomy.” 1993. Web. 19 Jan 2021.

Vancouver:

Trolliet Baumann, Maria Rosa 1. Hormonal and salt regulation of peripheral and brain renin-angiotensin system separated by nephrectomy. [Internet] [Thesis]. University of Florida; 1993. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00066672.

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

Council of Science Editors:

Trolliet Baumann, Maria Rosa 1. Hormonal and salt regulation of peripheral and brain renin-angiotensin system separated by nephrectomy. [Thesis]. University of Florida; 1993. Available from: https://ufdc.ufl.edu/AA00066672

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

Michigan State University

6. Asirvatham-jeyaraj, Ninitha-Margret-Julfiya. Role of central eicosanoids in the development of angiotensin ii-salt hypertension in the rat.

Degree: 2013, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:3336

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Thesis Ph. D. Michigan State University. Pharmacology and Toxicology - Doctor of Philosophy 2013.

Human essential hypertension (HTN) causes end organ damage, cardiovascular disease and… (more)

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Thesis Ph. D. Michigan State University. Pharmacology and Toxicology - Doctor of Philosophy 2013.

Human essential hypertension (HTN) causes end organ damage, cardiovascular disease and premature death. While increased sympathetic nerve activity (SNA) is a principal risk factor for the development of HTN, the central mechanisms that drive high sympathetic outflow remain unclear. Increased SNA and blood pressure (BP) can be triggered by high salt intake (2% NaCl) and the hormone angiotensin II (AngII). Our lab has extensively studied a rat model of HTN caused by these two factors in combination (AngII-salt HTN), and have shown that SNA contributes to the HTN and blocking whole-body eicosanoid (prostaglandin, thromboxane, lipoxygenase) synthesis with cyclooxygenase (COX) inhibitors attenuated both the increased SNA and HTN development. My project was to determine how eicosanoid products contribute to AngII-salt HTN. In initial experiments, I showed that whole-body COX inhibition failed to reverse established AngII-salt HTN in rats (similar to human hypertensives). In contrast, COX inhibition only during the first several days of 14-day AngII-salt treatment successfully prevented subsequent HTN development and sympathetic support of BP (i.e. neurogenic pressor activity). I concluded that COX products exert important physiological effects only during the early phase. I next investigated the roles of the two isoforms of COX and found that COX-1 specific products drive the development of AngII-salt HTN. Because most eicosanoid products in peripheral tissues (blood vessel, kidney) lower BP, I decided to test if central (i.e. brain) eicosanoids, acting early in the process of AngII-salt HTN development, cause a long-lived increase in SNA and BP. I chronically administered the COX inhibitor into the brain at a dose designed to block COX in the brain, and showed that this prevented increase in SNA and HTN development. I concluded that one or more COX-1 products in the brain contribute to HTN development. I also performed PCR and Western blot analysis of COX pathway-associated gene and protein expression in known cardio-regulatory regions of the brain. This revealed only modest changes for the most part, but I observed significant changes in the prostaglandin D2 (PGD2) pathway (downstream from COX) in the OVLT (cardio-regulatory brain region), choroid plexus (CP) and cerebrospinal fluid (CSF). Importantly, I showed increased lipocalin-prostaglandin D synthase (L-PGDS) expression in the CP and CSF, the main sites of L-PGDS synthesis and secretion, respectively. These findings were the first ever to implicate brain PGD2 in HTN. Thus, to investigate this finding in more detail, I measure brain levels of PGD2 with mass spectrometry and found high levels in CSF and rostral ventrolateral medulla (RVLM) of HTN rats. PGD2 in the brain binds mainly to the G-protein coupled receptor DP1R. Immunofluorescence staining revealed down-regulation of DP1R in the RVLM during the early phase of AngII-salt HTN; perhaps predictable in the…

Advisors/Committee Members: Fink, Gregory D, Mohankumar, Puliyur, Galligan, James, Northcott, Carrie, Xu, Hui.

Subjects/Keywords: Hypertension – Animal models; Eicosanoids; Angiotensin II; Cyclooxygenases; Pharmacology; Toxicology; Physiology; Ang II-salt HTN; COX

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

APA (6^th Edition):

Asirvatham-jeyaraj, N. (2013). Role of central eicosanoids in the development of angiotensin ii-salt hypertension in the rat. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:3336

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):

Asirvatham-jeyaraj, Ninitha-Margret-Julfiya. “Role of central eicosanoids in the development of angiotensin ii-salt hypertension in the rat.” 2013. Thesis, Michigan State University. Accessed January 19, 2021. http://etd.lib.msu.edu/islandora/object/etd:3336.

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

MLA Handbook (7^th Edition):

Asirvatham-jeyaraj, Ninitha-Margret-Julfiya. “Role of central eicosanoids in the development of angiotensin ii-salt hypertension in the rat.” 2013. Web. 19 Jan 2021.

Vancouver:

Asirvatham-jeyaraj N. Role of central eicosanoids in the development of angiotensin ii-salt hypertension in the rat. [Internet] [Thesis]. Michigan State University; 2013. [cited 2021 Jan 19]. Available from: http://etd.lib.msu.edu/islandora/object/etd:3336.

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

Council of Science Editors:

Asirvatham-jeyaraj N. Role of central eicosanoids in the development of angiotensin ii-salt hypertension in the rat. [Thesis]. Michigan State University; 2013. Available from: http://etd.lib.msu.edu/islandora/object/etd:3336

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

University of Florida

7. Richards-Sumners, Elaine Mary, 1957-. Catecholamine and angiotensin II interactions in primary cultures of brain cells.

Degree: 1988, University of Florida

URL: https://ufdc.ufl.edu/AA00054447

Subjects/Keywords: Brain; Catecholamines; Cultured cells; Incubation; Insulin; Neuroglia; Neurons; Norepinephrine; Rats; Receptors; Angiotensin II – physiology ( mesh ); Brain Chemistry ( mesh ); Catecholamines – physiology ( mesh ); Cells, Cultured ( mesh ); Physiology thesis Ph.D ( mesh )

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

APA (6^th Edition):

Richards-Sumners, Elaine Mary, 1. (1988). Catecholamine and angiotensin II interactions in primary cultures of brain cells. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00054447

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):

Richards-Sumners, Elaine Mary, 1957-. “Catecholamine and angiotensin II interactions in primary cultures of brain cells.” 1988. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00054447.

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

MLA Handbook (7^th Edition):

Richards-Sumners, Elaine Mary, 1957-. “Catecholamine and angiotensin II interactions in primary cultures of brain cells.” 1988. Web. 19 Jan 2021.

Vancouver:

Richards-Sumners, Elaine Mary 1. Catecholamine and angiotensin II interactions in primary cultures of brain cells. [Internet] [Thesis]. University of Florida; 1988. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00054447.

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

Council of Science Editors:

Richards-Sumners, Elaine Mary 1. Catecholamine and angiotensin II interactions in primary cultures of brain cells. [Thesis]. University of Florida; 1988. Available from: https://ufdc.ufl.edu/AA00054447

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

University of Florida

8. Paulding, Waltke Reche, 1964-. Regulation of atrial natriuretic peptide receptors in astroglia.

Degree: 1996, University of Florida

URL: https://ufdc.ufl.edu/AA00067432

Subjects/Keywords: Research ( mesh ); Receptors, Atrial Natriuretic Factor – physiology ( mesh ); Astrocytes ( mesh ); Cells, Cultured ( mesh ); Protein Kinase C – physiology ( mesh ); Angiotensin II – physiology ( mesh ); Rats, Sprague-Dawley ( mesh ); Rats, Inbred SHR ( mesh ); Rats, Inbred WKY ( mesh ); Department of Physiology thesis Ph.D ( mesh )

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

APA (6^th Edition):

Paulding, Waltke Reche, 1. (1996). Regulation of atrial natriuretic peptide receptors in astroglia. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00067432

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):

Paulding, Waltke Reche, 1964-. “Regulation of atrial natriuretic peptide receptors in astroglia.” 1996. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00067432.

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

MLA Handbook (7^th Edition):

Paulding, Waltke Reche, 1964-. “Regulation of atrial natriuretic peptide receptors in astroglia.” 1996. Web. 19 Jan 2021.

Vancouver:

Paulding, Waltke Reche 1. Regulation of atrial natriuretic peptide receptors in astroglia. [Internet] [Thesis]. University of Florida; 1996. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00067432.

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

Council of Science Editors:

Paulding, Waltke Reche 1. Regulation of atrial natriuretic peptide receptors in astroglia. [Thesis]. University of Florida; 1996. Available from: https://ufdc.ufl.edu/AA00067432

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

University of Florida

9. Li, Bing, 1962-. The Role of the renin-angiotensin system in the cerebral ischemia in a model of stroke.

Degree: 1996, University of Florida

URL: https://ufdc.ufl.edu/AA00052902

Subjects/Keywords: Antisense oligonucleotides; Blood flow; Blood pressure; Brain; Brain ischemia; Forebrain; Messenger RNA; Oligonucleotides; Rats; Receptors; Angiotensin II – metabolism ( mesh ); Biphenyl Compounds – pharmacology ( mesh ); Biphenyl Compounds – therapeutic use ( mesh ); Blood Pressure – physiology ( mesh ); Brain Ischemia – etiology ( mesh ); Brain Ischemia – physiopathology ( mesh ); Captopril – pharmacology ( mesh ); Captopril – therapeutic use ( mesh ); Carotid Arteries ( mesh ); Department of Physiology thesis Ph.D ( mesh ); Imidazoles – pharmacology ( mesh ); Imidazoles – therapeutic use ( mesh ); Ligation ( mesh ); Models, Cardiovascular ( mesh ); Oligonucleotides, Antisense – pharmacology ( mesh ); Oligonucleotides, Antisense – therapeutic use ( mesh ); Rats, Inbred SHR ( mesh ); Rats, Inbred WKY ( mesh ); Receptors, Angiotensin – metabolism ( mesh ); Renin-Angiotensin System – physiology ( mesh ); Research ( mesh ); Tetrazoles – pharmacology ( mesh ); Tetrazoles – therapeutic use ( mesh )

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

APA (6^th Edition):

Li, Bing, 1. (1996). The Role of the renin-angiotensin system in the cerebral ischemia in a model of stroke. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00052902

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, Bing, 1962-. “The Role of the renin-angiotensin system in the cerebral ischemia in a model of stroke.” 1996. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00052902.

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, Bing, 1962-. “The Role of the renin-angiotensin system in the cerebral ischemia in a model of stroke.” 1996. Web. 19 Jan 2021.

Vancouver:

Li, Bing 1. The Role of the renin-angiotensin system in the cerebral ischemia in a model of stroke. [Internet] [Thesis]. University of Florida; 1996. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00052902.

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

Council of Science Editors:

Li, Bing 1. The Role of the renin-angiotensin system in the cerebral ischemia in a model of stroke. [Thesis]. University of Florida; 1996. Available from: https://ufdc.ufl.edu/AA00052902

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

University of Florida

10. Olson, John Ackerman, 1964-. Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain.

Degree: 1990, University of Florida

URL: https://ufdc.ufl.edu/AA00022809

Subjects/Keywords: Astrocytes; Brain; Cell growth; Cells; Cultural studies; Cultured cells; Neurons; Rats; Receptors; Secretion; Angiotensin II – physiology ( mesh ); Astrocytes – growth &; development ( mesh ); Astrocytes – secretion ( mesh ); Brain Chemistry ( mesh ); Department of Pharmacology and Therapeutics thesis Ph.D ( mesh ); Insulin-Like Growth Factor-Binding Protein 2 ( mesh ); Proteins – secretion ( mesh ); Rats ( mesh ); Research ( mesh )

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APA (6^th Edition):

Olson, John Ackerman, 1. (1990). Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00022809

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):

Olson, John Ackerman, 1964-. “Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain.” 1990. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00022809.

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

MLA Handbook (7^th Edition):

Olson, John Ackerman, 1964-. “Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain.” 1990. Web. 19 Jan 2021.

Vancouver:

Olson, John Ackerman 1. Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain. [Internet] [Thesis]. University of Florida; 1990. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00022809.

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

Council of Science Editors:

Olson, John Ackerman 1. Developmental regulation of constitutive and angiotensin II-induced protein secretion by astrocytes of the brain. [Thesis]. University of Florida; 1990. Available from: https://ufdc.ufl.edu/AA00022809

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

University of Florida

11. Kopnisky, Kathy L., 1964-. Modulation of lipopolysaccharide and cytokine stimulated inducible nitric oxide synthase by angiotensin II.

Degree: 1996, University of Florida

URL: https://ufdc.ufl.edu/AA00052901

Subjects/Keywords: Astrocytes; Brain; Cytokines; Endotoxins; Messenger RNA; Microglia; Nitrites; Oxides; Rats; Receptors; Angiotensin II – pharmacology ( mesh ); Astrocytes ( mesh ); Cytokines ( mesh ); Department of Physiology thesis Ph.D ( mesh ); Endotoxins ( mesh ); Enzyme Induction ( mesh ); Enzyme Induction – drug effects ( mesh ); Interferon Type II ( mesh ); Interleukin-1 ( mesh ); Lipopolysaccharides ( mesh ); Nitric-Oxide Synthase – drug effects ( mesh ); Protein Kinase C – pharmacology ( mesh ); Rats ( mesh ); Research ( mesh ); Tumor Necrosis Factor ( mesh )

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

APA (6^th Edition):

Kopnisky, Kathy L., 1. (1996). Modulation of lipopolysaccharide and cytokine stimulated inducible nitric oxide synthase by angiotensin II. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00052901

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):

Kopnisky, Kathy L., 1964-. “Modulation of lipopolysaccharide and cytokine stimulated inducible nitric oxide synthase by angiotensin II.” 1996. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00052901.

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

MLA Handbook (7^th Edition):

Kopnisky, Kathy L., 1964-. “Modulation of lipopolysaccharide and cytokine stimulated inducible nitric oxide synthase by angiotensin II.” 1996. Web. 19 Jan 2021.

Vancouver:

Kopnisky, Kathy L. 1. Modulation of lipopolysaccharide and cytokine stimulated inducible nitric oxide synthase by angiotensin II. [Internet] [Thesis]. University of Florida; 1996. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00052901.

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

Council of Science Editors:

Kopnisky, Kathy L. 1. Modulation of lipopolysaccharide and cytokine stimulated inducible nitric oxide synthase by angiotensin II. [Thesis]. University of Florida; 1996. Available from: https://ufdc.ufl.edu/AA00052901

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

University of Edinburgh

12. 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 (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 January 19, 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. 19 Jan 2021.

Vancouver:

Ashek A. Altered renal function and the development of angiotensin II-dependent hypertension. [Internet] [Doctoral dissertation]. University of Edinburgh; 2011. [cited 2021 Jan 19]. 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

University of Florida

13. Reutter, Michael A., 1959-. Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter.

Degree: 1997, University of Florida

URL: https://ufdc.ufl.edu/AA00011813

Subjects/Keywords: Adrenergic receptors; Agonists; Astrocytes; Cell lines; Cultured cells; Inurement; Messenger RNA; Norepinephrine; Rats; Receptors; Angiotensin II ( mesh ); Astrocytes ( mesh ); Cells, Cultured ( mesh ); Cyclic AMP ( mesh ); Department of Physiology thesis Ph.D ( mesh ); Epinephrine ( mesh ); Gene Expression Regulation ( mesh ); Protein Kinase C ( mesh ); RNA, Messenger ( mesh ); Rats, Sprague-Dawley ( mesh ); Receptors, Adrenergic, alpha-2 – biosynthesis ( mesh ); Receptors, Adrenergic, alpha-2 – metabolism ( mesh ); Research ( mesh ); Signal Transduction ( mesh ); Transcription, Genetic ( mesh )

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APA (6^th Edition):

Reutter, Michael A., 1. (1997). Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00011813

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):

Reutter, Michael A., 1959-. “Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter.” 1997. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00011813.

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

MLA Handbook (7^th Edition):

Reutter, Michael A., 1959-. “Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter.” 1997. Web. 19 Jan 2021.

Vancouver:

Reutter, Michael A. 1. Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter. [Internet] [Thesis]. University of Florida; 1997. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00011813.

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

Council of Science Editors:

Reutter, Michael A. 1. Regulation of Alpha2A-Adrenergic receptor expression in cultured rat astroglia by Michael A. Reutter. [Thesis]. University of Florida; 1997. Available from: https://ufdc.ufl.edu/AA00011813

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

14. 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

►

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 (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 January 19, 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. 19 Jan 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 Jan 19]. 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

15. 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 (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 January 19, 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. 19 Jan 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 Jan 19]. 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

16. 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 (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 January 19, 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. 19 Jan 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 Jan 19]. 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 Florida

17. Curtis, Lisa M. Vacuolar H-ATPase and the nephron developmental apoptosis and adult physiology.

Degree: 2001, University of Florida

URL: https://ufdc.ufl.edu/AA00022185

Subjects/Keywords: Antibodies; Apoptosis; Arrows; Cell growth; Cell membranes; Cells; Kidney cortex; Kidneys; Rats; Receptors; Angiotensin II ( mesh ); Apoptosis ( mesh ); Department of Anatomy and Cell Biology thesis Ph.D ( mesh ); Nephrons – physiology ( mesh ); Proton-Translocating ATPases ( mesh ); rab GTP-Binding Proteins ( mesh )

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APA (6^th Edition):

Curtis, L. M. (2001). Vacuolar H-ATPase and the nephron developmental apoptosis and adult physiology. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00022185

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):

Curtis, Lisa M. “Vacuolar H-ATPase and the nephron developmental apoptosis and adult physiology.” 2001. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00022185.

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

MLA Handbook (7^th Edition):

Curtis, Lisa M. “Vacuolar H-ATPase and the nephron developmental apoptosis and adult physiology.” 2001. Web. 19 Jan 2021.

Vancouver:

Curtis LM. Vacuolar H-ATPase and the nephron developmental apoptosis and adult physiology. [Internet] [Thesis]. University of Florida; 2001. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00022185.

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

Council of Science Editors:

Curtis LM. Vacuolar H-ATPase and the nephron developmental apoptosis and adult physiology. [Thesis]. University of Florida; 2001. Available from: https://ufdc.ufl.edu/AA00022185

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

Western Kentucky University

18. Freeman, Julia Carol. Single Nucleotide Polymorphisms Linked to Essential Hypertension in Kasigau, Kenya.

Degree: MS, Department of Biology, 2013, Western Kentucky University

URL: https://digitalcommons.wku.edu/theses/1316

► Hypertension, or high blood pressure (BP), is an ever-growing epidemic in the developing world. Understanding the genetics behind essential hypertension (EH), or hypertension with… (more)

Subjects/Keywords: Angiotensinogen; Blood Pressure; Renin Angiotensin System; Angiotensin II Receptor; Isoform 1; Hydroxysteroid (11-beta) Dehydrogenase 2; Biology; Cardiology; Genetics; Medical Education; Physiology

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APA (6^th Edition):

Freeman, J. C. (2013). Single Nucleotide Polymorphisms Linked to Essential Hypertension in Kasigau, Kenya. (Masters Thesis). Western Kentucky University. Retrieved from https://digitalcommons.wku.edu/theses/1316

Chicago Manual of Style (16^th Edition):

Freeman, Julia Carol. “Single Nucleotide Polymorphisms Linked to Essential Hypertension in Kasigau, Kenya.” 2013. Masters Thesis, Western Kentucky University. Accessed January 19, 2021. https://digitalcommons.wku.edu/theses/1316.

MLA Handbook (7^th Edition):

Freeman, Julia Carol. “Single Nucleotide Polymorphisms Linked to Essential Hypertension in Kasigau, Kenya.” 2013. Web. 19 Jan 2021.

Vancouver:

Freeman JC. Single Nucleotide Polymorphisms Linked to Essential Hypertension in Kasigau, Kenya. [Internet] [Masters thesis]. Western Kentucky University; 2013. [cited 2021 Jan 19]. Available from: https://digitalcommons.wku.edu/theses/1316.

Council of Science Editors:

Freeman JC. Single Nucleotide Polymorphisms Linked to Essential Hypertension in Kasigau, Kenya. [Masters Thesis]. Western Kentucky University; 2013. Available from: https://digitalcommons.wku.edu/theses/1316

University of Western Ontario

19. Ghoreishi, Sina A. Nicotinamide Riboside and the Aortic Response to Angiotensin II Infusion in Mice.

Degree: 2017, University of Western Ontario

URL: https://ir.lib.uwo.ca/etd/4788

► Damage to vascular cells of the aorta drives vascular dysfunction and disease. Nicotinamide adenine dinucleotide (NAD+) is a cellular metabolite critical to cellular health, but… (more)

Subjects/Keywords: NAD+; nicotinamide riboside; angiotensin II; aorta; endothelial cells; vascular smooth muscle cells; Circulatory and Respiratory Physiology

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APA (6^th Edition):

Ghoreishi, S. A. (2017). Nicotinamide Riboside and the Aortic Response to Angiotensin II Infusion in Mice. (Thesis). University of Western Ontario. Retrieved from https://ir.lib.uwo.ca/etd/4788

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):

Ghoreishi, Sina A. “Nicotinamide Riboside and the Aortic Response to Angiotensin II Infusion in Mice.” 2017. Thesis, University of Western Ontario. Accessed January 19, 2021. https://ir.lib.uwo.ca/etd/4788.

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

MLA Handbook (7^th Edition):

Ghoreishi, Sina A. “Nicotinamide Riboside and the Aortic Response to Angiotensin II Infusion in Mice.” 2017. Web. 19 Jan 2021.

Vancouver:

Ghoreishi SA. Nicotinamide Riboside and the Aortic Response to Angiotensin II Infusion in Mice. [Internet] [Thesis]. University of Western Ontario; 2017. [cited 2021 Jan 19]. Available from: https://ir.lib.uwo.ca/etd/4788.

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

Council of Science Editors:

Ghoreishi SA. Nicotinamide Riboside and the Aortic Response to Angiotensin II Infusion in Mice. [Thesis]. University of Western Ontario; 2017. Available from: https://ir.lib.uwo.ca/etd/4788

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

University of Florida

20. Gyurko, Robert. Antisense inhibition of brain angiotensin in rat model of genetic hypertension.

Degree: 1995, University of Florida

URL: https://ufdc.ufl.edu/AA00020009

Subjects/Keywords: Antisense oligonucleotides; Blood pressure; Brain; Cells; DNA; Hypertension; Messenger RNA; Oligonucleotides; Rats; Receptors; Angiotensin II ( mesh ); Gene Expression Regulation ( mesh ); Hypertension ( mesh ); Oligonucleotides, Antisense – genetics ( mesh ); Oligonucleotides, Antisense – pharmacology ( mesh ); Receptors, Angiotensin ( mesh ); City of Gainesville ( local )

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APA (6^th Edition):

Gyurko, R. (1995). Antisense inhibition of brain angiotensin in rat model of genetic hypertension. (Thesis). University of Florida. Retrieved from https://ufdc.ufl.edu/AA00020009

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):

Gyurko, Robert. “Antisense inhibition of brain angiotensin in rat model of genetic hypertension.” 1995. Thesis, University of Florida. Accessed January 19, 2021. https://ufdc.ufl.edu/AA00020009.

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

MLA Handbook (7^th Edition):

Gyurko, Robert. “Antisense inhibition of brain angiotensin in rat model of genetic hypertension.” 1995. Web. 19 Jan 2021.

Vancouver:

Gyurko R. Antisense inhibition of brain angiotensin in rat model of genetic hypertension. [Internet] [Thesis]. University of Florida; 1995. [cited 2021 Jan 19]. Available from: https://ufdc.ufl.edu/AA00020009.

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

Council of Science Editors:

Gyurko R. Antisense inhibition of brain angiotensin in rat model of genetic hypertension. [Thesis]. University of Florida; 1995. Available from: https://ufdc.ufl.edu/AA00020009

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

University of Gothenburg / Göteborgs Universitet

21. Guron, Gregor 1967-. An intact renin-angiotensin system is essential for normal renal development.

Degree: 1998, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/11278

► The renin-angiotensin system (RAS) is important in the regulation of extracellular fluid volume and systemic blood pressure. In a previous study we accidentally found that… (more)

▼ The renin-angiotensin system (RAS) is important in the regulation of extracellular fluid volume and systemic blood pressure. In a previous study we accidentally found that pharmacological blockade of the RAS in neonatal rats with immature kidneys produced persistent renal morphological abnormalities. This observation suggested that the RAS, in addition to exerting its traditional functions in the control of circulatory homeostasis, may play a role in normal renal development. The aims of the present studies were to perform a detailed investigation of the consequences of neonatal inhibition of the RAS on long-term renal morphology and function in the rat. Moreover, we wanted to elucidate the specific postnatal time interval during which the rat kidney is vulnerable to an inhibition of the RAS, and whether our observations could be reproduced in a non-rodent kidney. Neonatal rats and piglets received daily intraperitoneal injections of the angiotensin-converting enzyme (ACE) inhibitor enalapril during the first 3 weeks after birth. Renal function was analyzed in adult rats using a combination of metabolic balance studies in conscious animals, and renal clearance experiments under anesthesia. Kidney histology was assessed with light microscopy using semiquantitative and stereological methods. ACE inhibition attenuated somatic growth in the neonate and produced persistent renal histopathological alterations characterized by papillary atrophy, interstitial fibrosis and chronic inflammation, tubular atrophy and dilatation, and wall thickening of interlobular arteries, in both rats and pigs. Functionally, adult rats subjected to neonatal ACE inhibition showed: an approximate 15 % reduction in glomerular filtration rate and effective renal plasma flow; an impaired urinary concentrating ability of renal origin; sodium retention during dietary sodium loading; and a modest and transient potassium wastage during dietary potassium restriction. In spite of the renal histological lesions, neonatally enalapril-treated rats displayed an intact sodium conservation during dietary sodium restriction and a preserved urinary acidification and net acid excretion. The renal lesions induced by enalapril did not seem to be the result of renal ischemia secondary to an arterial pressure reduction, as a blood pressure lowering control drug (nifedipine) did not produce any renal abnormalities. Postnatally, the rat kidney was vulnerable to ACE inhibition during the first 16 days specifically. The only renal abnormality associated with enalapril treatment after 14 days of age, i.e. after nephrogenesis had ceased, was a reduction in the volume fraction of tubular epithelium in the inner stripe of the outer medulla, which is the kidney zone last to mature, suggesting that angiotensin II may promote tubulogenesis at a stage in renal development when nephrogenesis has been completed. Taken together, the present studies demonstrate an essential role for the RAS in normal renal development. These findings underline that drugs which interrupt the RAS…

Subjects/Keywords: Angiotensin converting enzyme; angiotensin converting enzyme inhibitor; angiotensin II; kidney development; renal physiology; urine concentration; renal medulla

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

APA (6^th Edition):

Guron, G. 1. (1998). An intact renin-angiotensin system is essential for normal renal development. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/11278

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):

Guron, Gregor 1967-. “An intact renin-angiotensin system is essential for normal renal development.” 1998. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed January 19, 2021. http://hdl.handle.net/2077/11278.

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

MLA Handbook (7^th Edition):

Guron, Gregor 1967-. “An intact renin-angiotensin system is essential for normal renal development.” 1998. Web. 19 Jan 2021.

Vancouver:

Guron G1. An intact renin-angiotensin system is essential for normal renal development. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 1998. [cited 2021 Jan 19]. Available from: http://hdl.handle.net/2077/11278.

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

Council of Science Editors:

Guron G1. An intact renin-angiotensin system is essential for normal renal development. [Thesis]. University of Gothenburg / Göteborgs Universitet; 1998. Available from: http://hdl.handle.net/2077/11278

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

22. Gomes-Santos, Igor Lucas. Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética.

Degree: PhD, Cardiologia, 2014, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-04042014-162601/ ;

► INTRODUÇÃO: Capítulo 1. A Insuficiência Cardíaca (IC) é acompanhada de uma hiperativação simpática e do sistema renina-angiotensina (SRA). As ações deletérias do SRA são atribuídas… (more)

▼ INTRODUÇÃO: Capítulo 1. A Insuficiência Cardíaca (IC) é acompanhada de uma hiperativação simpática e do sistema renina-angiotensina (SRA). As ações deletérias do SRA são atribuídas à Angiotensina II (AngII), mas a Angiotensina-(1- 7) (Ang-(1-7)), um metabólito da AngII, demonstra efeitos cardiovasculares benéficos, contrários aos da AngII. O conceito tradicional é de que as concentrações sistêmicas mediam as respostas do SRA, mas evidências emergem acerca da importância funcional do SRA local. Nesse estudo, estudou-se o SRA circulante e muscular esquelético na IC, testando-se a hipótese de que as alterações seriam diferentes nesses dois territórios, e que o treinamento físico corrigiria essas alterações. Capítulo 2. A IC é uma síndrome sistêmica, onde fatores neuroendócrinos, como a AngII, podem levar a alterações periféricas. Na musculatura esquelética, a hiperatividade do sistema ubiquitina-proteassoma (SUP) é um dos elementos que compõem um quadro de miopatia, aumentando o catabolismo muscular em direção à atrofia, e contribuindo com o agravamento da síndrome. O treinamento físico normaliza o SUP e reduz as concentrações plasmáticas de AngII na IC. Dessa forma, testamos a hipótese de que a redução do SUP mediada pelo treinamento físico na IC depende da queda das concentrações plasmáticas de AngII. MÉTODOS: Capítulo 1. Ratos Wistar, machos, foram induzidos à IC por ligadura da artéria coronária descendente anterior, ou cirurgia fictícia (Sham, SH). Os animais foram divididos em grupos mantidos sedentários, SD (SHSD, n=10 e ICSD, n=12) ou submetidos ao treinamento físico, TR (SHTR, n=10, ICTR, n=12). O treinamento físico foi realizado em esteira, a 60% do consumo máximo de oxigênio, 5 dias por semana durante 8 semanas, quando foram sacrificados para coleta de sangue e músculos (sóleo e plantar). As angiotensinas circulantes e musculares foram dosadas por HPLC. A atividade sérica e muscular da ECA e da ECA2 por fluorimetria. Os receptores AT1 e AT2 foram analisados por expressão gênica (RT-PCR) e proteica (Western Blot), e o receptor Mas por expressão gênica. Capítulo 2. Ratos Wistar, machos, foram induzidos à IC por ligadura da artéria coronária descendente anterior, ou cirurgia fictícia (Sham). Após 4 semanas, os animais Sham (n=10) constituíram um grupo sedentário saudável (SHSD) e os animais com IC (n=30) foram igualmente alocados em 3 grupos: um mantido sedentário (ICSD), um treinado (ICTR) e um treinado com as concentrações plasmáticas de AngII nos mesmos níveis dos animais do grupo ICSD (ICTRAII), mantidas através de minipump osmótica. O treinamento físico foi realizado em esteira, a 60% do consumo máximo de oxigênio, 5 dias por semana durante 8 semanas, quando foram sacrificados para coleta de sangue e músculos (sóleo e plantar). As angiotensinas circulantes e musculares foram dosadas por HPLC. A expressão gênica das enzimas ligases E3?, MuRF e Atrogin foi realizada por RT-PCR. O receptor AT1, as proteínas ubiquitinadas e as proteínas carboniladas (Oxyblot) foram quantificadas por Western Blot. A atividade da… Advisors/Committee Members: Negrão, Carlos Eduardo.

Subjects/Keywords: Angiotensin II; Angiotensina II; Atrofia muscular/patologia; Atrofia muscular/reabilitação; Doenças musculares; Exercício/fisiologia; Exercise therapy; Exercise/physiology; Heart failure; Insuficiência cardíaca; Muscular atrophy/pathology; Muscular atrophy/rehabilitation; Muscular diseases; Ratos Wistar; Rats Wistar; Renin-angiotensin system; Sistema renina-angiotensina; Terapia por exercício; Ubiquitin/genetics; Ubiquitina/genética

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

APA (6^th Edition):

Gomes-Santos, I. L. (2014). Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/5/5131/tde-04042014-162601/ ;

Chicago Manual of Style (16^th Edition):

Gomes-Santos, Igor Lucas. “Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética.” 2014. Doctoral Dissertation, University of São Paulo. Accessed January 19, 2021. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-04042014-162601/ ;.

MLA Handbook (7^th Edition):

Gomes-Santos, Igor Lucas. “Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética.” 2014. Web. 19 Jan 2021.

Vancouver:

Gomes-Santos IL. Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética. [Internet] [Doctoral dissertation]. University of São Paulo; 2014. [cited 2021 Jan 19]. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-04042014-162601/ ;.

Council of Science Editors:

Gomes-Santos IL. Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética. [Doctoral Dissertation]. University of São Paulo; 2014. Available from: http://www.teses.usp.br/teses/disponiveis/5/5131/tde-04042014-162601/ ;

NSYSU

23. 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 January 19, 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. 19 Jan 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 Jan 19]. 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

24. 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 January 19, 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. 19 Jan 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 Jan 19]. 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

25. 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…

3 more images…

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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 January 19, 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. 19 Jan 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 Jan 19]. 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

26. 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 January 19, 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. 19 Jan 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 Jan 19]. 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

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

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 January 19, 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. 19 Jan 2021.

Vancouver:

Latchford KJ. Electrophysiological Effects of Angiotensin II on Hypothalamic Paraventricular Nucleus Neurons of the Rat . [Internet] [Thesis]. Queens University; 2008. [cited 2021 Jan 19]. 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

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

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 January 19, 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. 19 Jan 2021.

Vancouver:

Wahlberg K. The Role of Angiotensin II in Skeletal Muscle Metabolism. [Internet] [Masters thesis]. Virginia Tech; 2011. [cited 2021 Jan 19]. 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

29. Daubert, Daisy L. Decreased baroreflex gain during pregnancy : role of angiotensin II, nitric oxide and insulin sensitivity.

Degree: PhD, 2006, Oregon Health Sciences University

URL: doi:10.6083/M4SJ1HV8 ; http://digitalcommons.ohsu.edu/etd/2935

Subjects/Keywords: Baroreflex – physiology; Pregnancy; Insulin Resistance – physiology; Nitric Oxide – physiology; Angiotensin II – physiology; Rabbits – physiology

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APA (6^th Edition):

Daubert, D. L. (2006). Decreased baroreflex gain during pregnancy : role of angiotensin II, nitric oxide and insulin sensitivity. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4SJ1HV8 ; http://digitalcommons.ohsu.edu/etd/2935

Chicago Manual of Style (16^th Edition):

Daubert, Daisy L. “Decreased baroreflex gain during pregnancy : role of angiotensin II, nitric oxide and insulin sensitivity.” 2006. Doctoral Dissertation, Oregon Health Sciences University. Accessed January 19, 2021. doi:10.6083/M4SJ1HV8 ; http://digitalcommons.ohsu.edu/etd/2935.

MLA Handbook (7^th Edition):

Daubert, Daisy L. “Decreased baroreflex gain during pregnancy : role of angiotensin II, nitric oxide and insulin sensitivity.” 2006. Web. 19 Jan 2021.

Vancouver:

Daubert DL. Decreased baroreflex gain during pregnancy : role of angiotensin II, nitric oxide and insulin sensitivity. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 2006. [cited 2021 Jan 19]. Available from: doi:10.6083/M4SJ1HV8 ; http://digitalcommons.ohsu.edu/etd/2935.

Council of Science Editors:

Daubert DL. Decreased baroreflex gain during pregnancy : role of angiotensin II, nitric oxide and insulin sensitivity. [Doctoral Dissertation]. Oregon Health Sciences University; 2006. Available from: doi:10.6083/M4SJ1HV8 ; http://digitalcommons.ohsu.edu/etd/2935

30. 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 January 19, 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. 19 Jan 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 Jan 19]. 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/ ;

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