Effects of gender on the renin-Angiotensin system, blood pressure, and renal function

Kang, Amrit K.; Miller, Judith

doi:10.1007/s11906-002-0039-9

Cited by 32 publications

(26 citation statements)

References 57 publications

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“…However, both in humans and animal models, it has been well documented that males have a higher blood pressure and prevalence of end stage renal disease than age matched females. 32 In the present study, a higher proportion of male patients were hypertensive as compared with female patients at the baseline, although gender was not identified as an independent risk factor for PRD and the difference was not statistically significant. The reason for this gender difference in humans is unknown, but animal models have provided insights into potential mechanisms.…”

Section: Discussioncontrasting

confidence: 66%

Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy

Song¹,

Narita²,

Goto³

et al. 2003

Journal of Medical Genetics

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Section: Discussioncontrasting

confidence: 66%

Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy

Song¹,

Narita²,

Goto³

et al. 2003

Journal of Medical Genetics

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“…From that age on, a sexual dimorphism with higher blood and glomerular capillary pressure and increased protein excretion in males compared with age-matched females was reported in different hypertensive and normotensive rat strains (50). Androgens stimulate the systemic, as well as the local, renal RAS (51)(52)(53). AngII as a critical determinant of glomerular capillary pressure could therefore mediate the androgeninduced higher glomerular pressure in males.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor Overexpression in Podocytes Induces Glomerulosclerosis in Transgenic Rats

Hoffmann¹,

Podlich²,

Hähnel³

et al. 2004

Journal of the American Society of Nephrology

184

155

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Abstract. Angiotensin II (AngII) is a critical determinant of glomerular function involving both hemodynamic and pressure-independent effects that are insufficiently understood. A novel transgenic rat (TGR) model with overexpression of the human AngII type 1 receptor (hAT1) in podocytes was developed to study the consequences of an increased AT1 signaling on the structure and function of the glomerular filter. Use of the nephrin promoter to target the podocytes resulted in an expression of the hAT1 at a level roughly two times higher than the endogenous AT1 throughout life. All male TGR developed significant albuminuria starting at 8 to 15 wk of age; systolic BP was not elevated. More or less concurrently, structural changes at the glomerulus were encountered, starting with ubiquitous formation of pseudocysts at podocytes, followed by foot process effacement and local detachments. This damage progressed to nephron loss via the well known pathway typical for classic focal segmental glomerulosclerosis. The structural changes significantly correlated with age (r 2 ϭ 0.76) and urinary albumin excretion (r 2 ϭ 0.70). The data provide direct evidence that increased AT1 signaling in podocytes leads to protein leakage and structural podocyte damage progressing to focal segmental glomerulosclerosis.Angiotensin II (AngII) is the major effector molecule of the renin angiotensin system (RAS) acting as a circulating hormone as well as in a paracrine/autocrine fashion to modulate renal function. Activation of the RAS exacerbates progression to end-stage renal disease, and interruption of the RAS markedly retards proteinuria and advancement to nephrosclerosis (1,2). These effects appear to be based on at least two mechanisms: first, on the lowering of glomerular capillary pressure, and second, on pressure-independent mechanisms that are poorly understood. Podocytes have taken center stage as players in the progression of chronic renal disease. They express both AngII receptors, type 1 (AT1) and type 2 (AT2) (3,4). In glomerular disease models, blocking of AngII either by angiotensin converting enzyme inhibitors or AT1 antagonists prevented protein leakage and inhibited molecular changes in podocytes that otherwise occurred under the experimental conditions (5,6). Therefore, we speculated that AngII stimulation of podocytes via AT1 interferes with the barrier function and increases the vulnerability of podocytes to stress. To test this hypothesis, we developed a novel transgenic rat (TGR) model that overexpresses AT1 specifically and exclusively on podocytes. We found that increased AT1 signaling in podocytes leads to protein leakage and structural podocyte damage progressing to focal segmental glomerulosclerosis (FSGS). Materials and Methods Generation of TGRA 1.4-kb fragment of the human AT1 (hAT1) cDNA containing the entire coding region as well as 260 bp of the 5' and 64 bp of the 3' flanking regions (a gift from T. Inagami) were subcloned in between the 1.25-kb fragment of the human nephrin promoter (NPHS1) in PCR2.1 vecto...

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“…Sex differences in blood pressure are also evident in experimental models and human subjects, yet the mechanisms underlying this disparity remain equivocal [4,5,6,7]. The characterization of sex-based differences in experimental models of hypertension has focused on the components of the circulating renin-angiotensin system (RAS) [7,8,9]. The RAS not only plays a critical role in blood pressure control, but is also involved in learning and memory mechanisms [10,11,12].…”

Section: Introductionmentioning

confidence: 99%

Different Isoforms of Nitric Oxide Synthase Are Involved in Angiotensin-(1–7)-Mediated Plasticity Changes in the Amygdala in a Gender-Dependent Manner

Staschewski¹,

Kulisch²,

Albrecht³

2011

Neuroendocrinology

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Background: The amygdala receives afferent sensory input and processes information related to hydromineral balance. Angiotensin acts on and through the amygdala to stimulate thirst and sodium appetite. In addition, different angiotensins seem to play a role in cognition and learning mechanisms by acting on and through the amygdala. Recently, we showed that angiotensin-(1–7) (Ang-(1–7)) enhances the magnitude of long-term potentiation (LTP) in the lateral nucleus of the amygdala (LA) via the Mas receptor. Methods: Extracellular field potentials were measured in the LA. Results: LA-LTP induced by stimulation of the external capsule was nitric oxide (NO)-dependent because the NO synthase (NOS) inhibitor L-NAME reduced LA-LTP. The LA-LTP was also reduced in both male and female nNOS and eNOS knockout mice. In male eNOS^–/– mice, Ang-(1–7) enhanced LA-LTP, whereas the LTP-enhancing effect of Ang-(1–7) was missing in female eNOS^–/– mice. Therefore, the LTP-enhancing effect of Ang-(1–7) was mediated by eNOS in females. In contrast, Ang-(1–7) strongly enhanced the LTP in nNOS^–/– females, whereas the effect of Ang-(1–7) was missing in nNOS^–/– males. Thus, Ang-(1–7) induced an increase in the magnitude of LTP via the involvement of nNOS in males. Conclusion: Our data support not only the hypothesis that NO contributes to plasticity changes in the lateral amygdala, but also show for the first time a gender-dependent involvement of different isoforms of NOS in the mediation of Ang-(1–7) on LTP in the amygdala.

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Effects of gender on the renin-Angiotensin system, blood pressure, and renal function

Cited by 32 publications

References 57 publications

Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy

Gender specific association of aldosterone synthase gene polymorphism with renal survival in patients with IgA nephropathy

Angiotensin II Type 1 Receptor Overexpression in Podocytes Induces Glomerulosclerosis in Transgenic Rats

Different Isoforms of Nitric Oxide Synthase Are Involved in Angiotensin-(1–7)-Mediated Plasticity Changes in the Amygdala in a Gender-Dependent Manner

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