Gender modulates activation of renin-angiotensin and  endothelin systems in hypertension and heart failure

Radin, M. Judith; Holycross, Bethany J.; Sharkey, Leslie C.; Shiry, Laura; McCune, Sylvia A.

doi:10.1152/japplphysiol.00558.2001

Cited by 32 publications

(26 citation statements)

References 32 publications

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“…Renin-und Proreninspiegel sind bei Frauen niedriger als bei Män-nern und bei Frauen unter Hormonersatztherapie niedriger als bei Frauen ohne Hormonersatztherapie [9, 12]. Bei Herzinsuffizienz im Tiermodell war die Aktivierung des RAS bei älteren im Vergleich zu jüngeren Weibchen gesteigert [35]. Sowohl in Tiermodellen als auch bei Menschen konnte gezeigt werden, dass Östro-gene die Expression von AT1-Rezeptoren steigern und den AT2-Rezeptor in verschiedenen Gewebetypen wie z.…”

Section: Schlüsselfunktion Des Renin-angiotensin-systemsunclassified

Heart failure – are there gender aspects?

Regitz‐Zagrosek

Lehmkuhl

2008

Internist

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Gender differences in the syndrome of heart failure (HF) occur in etiology and pathophysiology, in the clinical presentation and course of the syndrome. In addition, gender specific treatment responses and gender associated differences in the behavior of treating physicians are found. Hypertension and diabetes play a major role as causes of HF in women and both interact in their pathophysiology with the renin angiotensin system (RAS). Modulation of the RAS by estrogens explains specific differences between pre- and postmenopausal women and men. Myocardial growth processes and myocardial calcium handling are differentially regulated in female and male myocytes. Myocardial remodeling with age and as a consequence of mechanical load differs in women and men. For yet unknown reasons, HF with preserved systolic function seems to be more frequent in women than in men and the clinical course of systolic failure is different in both genders.

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Section: Schlüsselfunktion Des Renin-angiotensin-systemsunclassified

Heart failure – are there gender aspects?

Regitz‐Zagrosek

Lehmkuhl

2008

Internist

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“…In diabetic patients with hypertension, endogenous inhibitors of NO synthase (NOS) can decrease the production of NO that acts as a vasodilator (16,39). In addition to effects on the vasculature, NO affects control of breathing directly by modulating neurotransmitter function in the carotid body and brain stem sites and/or possibly indirectly by decreasing blood pressure (10,12,22,30,32).To determine the efficacy of ACE inhibitors and Arg on diabetes and hypertension, we utilized the obese male spontaneously hypertensive heart failure (SHHF)/MccGmi-fa cp rat that develops noninsulin-dependent diabetes mellitus, obesity, hypertension, heart failure, and renal dysfunction (15,22,28,38). The "fa cp " designation reflects that the fatty (fa) gene mutation and corpulent (cp) obesity gene mutations are allelic.…”

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confidence: 99%

“…Obesity is an autosomal recessive trait expressed in only one of four pups, with the others expressing the lean phenotype. Obese male SHHF rats develop overt noninsulin-dependent diabetes mellitus with fasting hyperglycemia, hyperinsulinemia, hypercholesterolemia, hypertriglyceridemia, and abnormal glucose tolerance (28,38). In addition, the obese SHHF rats exhibit pronounced proteinuria, renal glomerular lesions consistent with diabetic nephropathy, and clinical signs of heart failure (enlarged hearts, generalized edema, and dyspnea), and they die at an earlier age than their lean littermates (28).…”

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confidence: 99%

“…To determine the efficacy of ACE inhibitors and Arg on diabetes and hypertension, we utilized the obese male spontaneously hypertensive heart failure (SHHF)/MccGmi-fa cp rat that develops noninsulin-dependent diabetes mellitus, obesity, hypertension, heart failure, and renal dysfunction (15,22,28,38). The "fa cp " designation reflects that the fatty (fa) gene mutation and corpulent (cp) obesity gene mutations are allelic.…”

mentioning

confidence: 99%

“…The ventricular failure leads to right ventricular hypertrophy and ultimately biventricular heart failure at 10 -12 mo of age. The obese SHHF male rat was chosen because it closely resembles the human condition in which metabolic disorders often cluster with hypertension (38). We had several hypotheses for this study.…”

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Effects of long-term captopril andl-arginine treatment on ventilation and blood pressure in obese male SHHF rats

Schlenker

Kost

Likness

2004

Journal of Applied Physiology

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Schlenker, E. H., C. K. Kost, Jr., and M. M. Likness. Effects of long-term captopril and L-arginine treatment on ventilation and blood pressure in obese male SHHF rats. J Appl Physiol 97: 1032-1039, 2004. First published May 14, 2004 10.1152/japplphysiol.00255.2004We investigated the effects of captopril (Cap) and L-arginine (Arg) on hypertension and cardiopulmonary function. Our hypothesis was that Cap therapy or Arg will improve cardiopulmonary risk factors for hypertension and hypoventilation in the obese spontaneously hypertensive heart failure rat, which is characterized by hypertension, obesity, and disorders of lipid and carbohydrate metabolism. For the first study, one group of rats received Cap in drinking water, and a second group received deionized water (DI). For the second study, rats were further subdivided. Some Cap-treated rats continued on this treatment, and the other half were now given DI to determine whether there would be residual effects of Cap treatment. A subgroup of rats who had received DI was then given Arg, whereas the rest remained on DI. In the first study, Cap-treated rats exhibited decreases in systolic and diastolic blood pressures, frequency of breathing, and minute ventilation, but ventilatory control was maintained. In contrast, blood pressures and relative ventilation to metabolism were higher in the DI-treated group. Removal of Cap increased blood pressure and decreased tidal volume while these rats maintained frequency. Although Arg-treated rats did not exhibit a decrease of blood pressure, ventilation was maintained in this group by preserving tidal volume. Thus Cap and Arg affected ventilation through different mechanisms independent of blood pressure.spontaneously hypertensive heart failure rat; hypertension; metabolic syndrome X; ventilatory equivalent; frequency OBESITY, DIABETES, AND HYPERTENSION are major risk factors for cardiopulmonary and renal disease (1,7,9,18,41). The concurrence of these risk factors is also known as the metabolic syndrome X (8, 49). In addition to metabolic and cardiovascular complications, individuals with metabolic syndrome X can also present with hypoventilation during sleep and obstructive sleep apnea (8, 47).Hypertension and congestive heart failure originate from the activation of multiple neuroendocrine systems, including the renin-angiotensin (Ang), endothelin, and atrial natriuretic peptide systems (13, 23-25, 41, 51). One in four adults develops hypertension and is at increased risk of stroke, coronary disease, congestive heart failure, and end-stage renal disease (2). Ang-converting enzyme (ACE) inhibitors are regarded as the first line of hypertensive therapy in diabetic patients due to their protective effects on the cardiovascular and renal systems (23,27,45). Ideally, treatment of hypertension would normalize blood pressure early in the disease, thus decreasing the incidence of cardiovascular-associated morbidity and mortality. Another agent that has been shown to decrease blood pressure is L-arginine (Arg) (50), a substrate ...

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Gender and Cardiovascular Diseases in Aging

Marı́n-Garcı́a

Goldenthal

Moe

Aging and the Heart

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Gender modulates activation of renin-angiotensin and endothelin systems in hypertension and heart failure

Cited by 32 publications

References 32 publications

Heart failure – are there gender aspects?

Heart failure – are there gender aspects?

Effects of long-term captopril andl-arginine treatment on ventilation and blood pressure in obese male SHHF rats

Gender and Cardiovascular Diseases in Aging

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