Document Detail


Role of androgens in mediating hypertension and renal injury.
MedLine Citation:
PMID:  10065333     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Men are generally at greater risk for cardiovascular disease than are women, particularly with regard to enhanced progression of hypertension and loss of renal function. Despite these gender differences in the progression of hypertension and renal disease in humans and animals, the mechanisms responsible are unknown. 2. Castration in males has been shown to slow the progression of hypertension and ameliorate the loss in renal function. When serum testosterone was measured in the developing male spontaneously hypertensive rat (SHR), the peak serum testosterone level at 12 weeks coincided with the time when differences in systolic blood pressure could be measured between intact male SHR and females or castrated male SHR. Ovariectomy does not affect blood pressure in female SHR but testosterone treatment of ovariectomized females for 5 weeks results in exacerbation of hypertension almost to the level found in intact male SHR. These data strongly suggest a role for androgens in mediating the gender differences in hypertension. 3. The mechanisms by which androgens could increase blood pressure are not known. We have recently shown that, at comparable renal perfusion pressures, there is a hypertensive shift in the pressure-natriuresis relationship in male SHR compared with females or castrated male SHR. Testosterone treatment of ovariectomized female SHR also causes a rightward shift in the pressure-natriuresis relationship. 4. We hypothesize that androgens increase arterial pressure by causing a hypertensive shift in the pressure-natriuresis relationship, either by having a direct effect to increase proximal tubular reabsorption or by activation of the renin-angiotensin system. We also hypothesize that the enhanced proximal tubular reabsorption leads to a tubuloglomerular feedback-mediated afferent vasodilation, which, in combination with the increase in arterial pressure, results in glomerular hypertension and renal injury.
Authors:
J F Reckelhoff; J P Granger
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Clinical and experimental pharmacology & physiology     Volume:  26     ISSN:  0305-1870     ISO Abbreviation:  Clin. Exp. Pharmacol. Physiol.     Publication Date:  1999 Feb 
Date Detail:
Created Date:  1999-06-09     Completed Date:  1999-06-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0425076     Medline TA:  Clin Exp Pharmacol Physiol     Country:  AUSTRALIA    
Other Details:
Languages:  eng     Pagination:  127-31     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505, USA. jfr@fiona.umsmed.edu
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MeSH Terms
Descriptor/Qualifier:
Androgens / physiology*
Animals
Cardiovascular Diseases / etiology*
Disease Progression
Female
Humans
Hypertension / etiology*
Kidney Diseases / etiology*
Male
Natriuresis / physiology
Rats
Rats, Inbred SHR
Rats, Sprague-Dawley
Receptors, Androgen / physiology
Renin-Angiotensin System / physiology
Sex Characteristics*
Testosterone / physiology
Grant Support
ID/Acronym/Agency:
HL 38499/HL/NHLBI NIH HHS; HL 51971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Androgens; 0/Receptors, Androgen; 58-22-0/Testosterone

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