Gender differences in development of hypertension in spontaneously hypertensive rats - Role of the renin-angiotensin system

Citation
Jf. Reckelhoff et al., Gender differences in development of hypertension in spontaneously hypertensive rats - Role of the renin-angiotensin system, HYPERTENSIO, 35(1), 2000, pp. 480-483
Citations number
36
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194-911X → ACNP
Volume
35
Issue
1
Year of publication
2000
Part
2
Supplement
S
Pages
480 - 483
Database
ISI
SICI code
0194-911X(200001)35:1<480:GDIDOH>2.0.ZU;2-1
Abstract
Previous data strongly support a role for androgens in promoting the gender difference in hypertension in the spontaneously hypertensive rat(s) (SHR), but the mechanism is not clear. Because males develop higher blood pressur es than do females, we hypothesize that androgens may affect the renin-angi otensin system to promote the development of hypertension in male SHR. The present study was performed to determine the effect of converting enzyme in hibition (CEI) on the development of hypertension in SHR. Male, female, cas trated male, and ovariectomized (ovx) female SHR (n=10 per gender per treat ment group) received enalapril (250 mg/L) in drinking water for 8 to 10 wee ks. Some ovx females were also given testosterone chronically. At 17 to 19 weeks of age, 24-hour protein excretion and mean arterial pressure were mea sured. By 13 weeks of age, male rats had higher systolic blood pressures by tail plethysmography than did the other rats, and CEI reduced blood pressu res to similar levels in all groups. At 17 to 19 weeks, the same trend was found by direct measurement of mean arterial pressure. The ovx females trea ted with. testosterone had serum testosterone and blood pressure levels sim ilar to those found in males. CEI reduced mean arterial pressure to similar levels in all gender groups. Untreated males and ovx females given testost erone had significantly higher levels of urinary protein excretion than did the other groups, and CEI had no effect on proteinuria in any of the rats. These data suggest that the development of hypertension in SHR regardless of sex steroids is mediated by the renin-angiotensin system. However, the d ata further suggest that androgens promote the exacerbation of hypertension in male SHR via a mechanism involving the renin-angiotensin system.