Perinatal Taurine Depletion Alters the Renal Excretory Effect of the Renin-Angiotensin System in Adult Female Rats

2015 ◽  
pp. 679-691 ◽  
Author(s):  
Wichaporn Lerdweeraphon ◽  
J. Michael Wyss ◽  
Thidarut Boonmars ◽  
Sanya Roysommuti
Keyword(s):  
Adult Female ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Central endogenous angiotensin-(1–7) protects against aldosterone/NaCl-induced hypertension in female rats

2013 ◽  
Vol 305 (5) ◽  
pp. H699-H705 ◽  
Author(s):  
Baojian Xue ◽  
Zhongming Zhang ◽  
Ralph F. Johnson ◽  
Fang Guo ◽  
Meredith Hay ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Inhibitory Effect ◽  
Protective Role ◽  
Female Rats ◽  
Pressor Effect ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Female Sex Hormones ◽  
Induced Hypertension

In comparison to male rodents, females are protected against angiotensin (ANG) II- and aldosterone (Aldo)-induced hypertension. However, the mechanisms underlying this protective effect are not well understood. ANG-(1–7) is formed from ANG II by angiotensin-converting enzyme 2 (ACE2) and has an antihypertensive effect in the central nervous system (CNS). The present study tested the hypothesis that central ANG-(1–7) plays an important protective role in attenuating the development of Aldo/NaCl-hypertension in female rats. Systemic infusion of Aldo into intact female rats with 1% NaCl as their sole drinking fluid resulted in a slight increase in blood pressure (BP). Intracerebroventricular (icv) infusion of A-779, an ANG-(1–7) receptor (Mas-R) antagonist, significantly augmented the pressor effects of Aldo/NaCl. In contrast, systemic Aldo/NaCl induced a significant increase in BP in ovariectomized (OVX) female rats, and central infusion of ANG-(1–7) significantly attenuated this Aldo/NaCl pressor effect. The inhibitory effect of ANG-(1–7) on the Aldo/NaCl pressor effect was abolished by concurrent infusion of A-779. RT-PCR analyses showed that there was a corresponding change in mRNA expression of several renin-angiotensin system components, estrogen receptors and an NADPH oxidase subunit in the lamina terminalis. Taken together these results suggest that female sex hormones regulate an antihypertensive axis of the brain renin-angiotensin system involving ACE2/ANG-(1–7)/Mas-R that plays an important counterregulatory role in protecting against the development of Aldo/NaCl-induced hypertension.

Vasoactive drugs enhance pancreatic islet blood flow, augment insulin secretion and improve glucose tolerance in female rats

2006 ◽  
Vol 112 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Zhen Huang ◽  
Leif Jansson ◽  
Åke Sjöholm
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Insulin Secretion ◽  
Glucose Tolerance ◽  
Pancreatic Islet ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Islet Blood Flow

Pravastatin, irbesartan and captopril are frequently used in the treatment of patients with Type 2 diabetes. These drugs also exert beneficial metabolic effects, causing an improved glucose tolerance in patients, but the precise mechanisms by which this is achieved remain elusive. To this end, we have studied whether these drugs influence insulin secretion in vivo through effects on islet blood perfusion. Captopril (3 mg/kg of body weight), irbesartan (3 mg/kg of body weight) and pravastatin (0.5 mg/kg of body weight) were injected intravenously into anaesthetized female Wistar rats. Blood flow rates were determined by a microsphere technique. Blood glucose concentrations were measured with test reagent strips and serum insulin concentrations were measured by ELISA. Pancreatic blood flow was markedly increased by pravastatin (P<0.001), captopril (P<0.05) and irbesartan (P<0.01). Pancreatic islet blood flow was significantly and preferentially enhanced after the administration of captopril (P<0.01), irbesartan (P<0.01) and pravastatin (P<0.001). Kidney blood flow was enhanced significantly by pravastatin (P<0.01), irbesartan (P<0.05) and captopril (P<0.01). Captopril and pravastatin also enhanced late-phase insulin secretion and positively influenced glycaemia in intraperitoneal glucose tolerance tests. In conclusion, the present study suggests that a local pancreatic renin–angiotensin system and pravastatin treatment may be selectively controlling pancreatic islet blood flow, augmenting insulin secretion and thereby improving glucose tolerance. Our findings indicate significant gender-related differences in the vascular response to these agents. Since statins and renin–angiotensin system inhibitors are frequently used by diabetic patients, the antidiabetic actions of these drugs reported previously might occur, in part, through the beneficial direct islet effects shown in the present study.

scholarly journals Long-Lasting Androgen-Induced Cardiometabolic Effects in Polycystic Ovary Syndrome

2018 ◽  
Vol 2 (8) ◽  
pp. 949-964 ◽  
Author(s):  
Edgar D Torres Fernandez ◽  
Kristen V Adams ◽  
Maryam Syed ◽  
Rodrigo O Maranon ◽  
Damian G Romero ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Ovary Syndrome ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Clinical Scenarios ◽  
Androgen Levels

Abstract Polycystic ovary syndrome (PCOS), the most common endocrine disorder in women of reproductive age, is characterized by androgen excess and ovarian dysfunction and presents with increased cardiometabolic risk factors such as obesity, insulin resistance, and elevated blood pressure (BP). We previously reported that administration of dihydrotestosterone (DHT) to female rats elicits cardiometabolic derangements similar to those found in women with PCOS. In this study, we tested the hypothesis that the DHT-mediated cardiometabolic derangements observed in PCOS are long lasting despite DHT withdrawal. Four-week-old female Sprague Dawley rats were treated with DHT (7.5 mg/90 days) or placebo for 6 months. DHT was discontinued (ex-DHT), and rats were followed for 6 additional months. After 6 months of DHT withdrawal, food intake, body weight, fat and lean mass, fasting plasma insulin, leptin, and adiponectin were elevated in ex-DHT rats. BP remained significantly elevated, and enalapril, an angiotensin-converting enzyme (ACE) inhibitor, normalized BP in ex-DHT rats. Expression of components of the intrarenal renin-angiotensin system was increased in ex-DHT rats. The cardiometabolic features found in ex-DHT rats were associated with lower plasma androgen levels but increased expression of renal and adipose tissue androgen receptors. In summary, androgen-induced cardiometabolic effects persisted after DHT withdrawal in a PCOS experimental model. Activation of intrarenal renin-angiotensin system plays a major role in the androgen-mediated increase in BP in ex-DHT. Upregulation of the renal and adipose tissue androgen receptor may explain the long-lasting effects of androgens. In clinical scenarios characterized by hyperandrogenemia in women, prompt normalization of androgen levels may be necessary to prevent their long-lasting cardiometabolic effects.

scholarly journals Estrogen regulation of the brain renin-angiotensin system in protection against angiotensin II-induced sensitization of hypertension

2014 ◽  
Vol 307 (2) ◽  
pp. H191-H198 ◽  
Author(s):  
Baojian Xue ◽  
Zhongming Zhang ◽  
Terry G. Beltz ◽  
Fang Guo ◽  
Meredith Hay ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Ang Ii ◽  
Central Administration ◽  
Estrogen Regulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Intracerebroventricular Infusion ◽  
Male And Female Rats

This study investigated sex differences in the sensitization of angiotensin (ANG) II-induced hypertension and the role of central estrogen and ANG-(1–7) in this process. Male and female rats were implanted for telemetered blood pressure (BP) recording. A subcutaneous subpressor dose of ANG II was given alone or concurrently with intracerebroventricular estrogen, ANG-(1–7), an ANG-(1–7) receptor antagonist A-779 or vehicle for 1 wk (induction). After a 1-wk rest (delay), a pressor dose of ANG II was given for 2 wk (expression). In males and ovariectomized females, subpressor ANG II had no sustained effect on BP during induction, but produced an enhanced hypertensive response to the subsequent pressor dose of ANG II during expression. Central administration of estrogen or ANG-(1–7) during induction blocked ANG II-induced sensitization. In intact females, subpressor ANG II treatment produced a decrease in BP during induction and delay, and subsequent pressor ANG II treatment given during expression produced only a slight but significant increase in BP. However, central blockade of ANG-(1–7) by intracerebroventricular infusion of A-779 during induction restored the decreased BP observed in females during induction and enhanced the pressor response to the ANG II treatment during expression. RT-PCR analyses indicated that estrogen given during induction upregulated mRNA expression of the renin-angiotensin system (RAS) antihypertensive components, whereas both central estrogen and ANG-(1–7) downregulated mRNA expression of RAS hypertensive components in the lamina terminalis. The results indicate that females are protected from ANG II-induced sensitization through central estrogen and its regulation of brain RAS.

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