Gender and the renin-angiotensin-aldosterone system

被引：229

作者：

Komukai, Kimiaki ^{[1
]}

Mochizuki, Seibu ^{[2
]}

Yoshimura, Michihiro ^{[1
]}

机构：

[1] Jikei Univ, Sch Med, Div Cardiol, Minato Ku, Tokyo 1058461, Japan

[2] Musashino Univ, Med Ctr, Minato Ku, Tokyo 1080075, Japan

来源：

FUNDAMENTAL & CLINICAL PHARMACOLOGY | 2010年 / 24卷 / 06期

关键词：

androgens; angiotensin receptor; natriuretic peptides; oestrogen; SPONTANEOUSLY HYPERTENSIVE-RATS; HORMONE REPLACEMENT THERAPY; CONVERTING-ENZYME-INHIBITORS; AMBULATORY BLOOD-PRESSURE; MESSENGER-RNA EXPRESSION; NORMOTENSIVE POSTMENOPAUSAL WOMEN; AT(1) RECEPTOR EXPRESSION; ESTROGEN PLUS PROGESTIN; CHRONIC-RENAL-FAILURE; SALT-SENSITIVE RATS;

D O I：

10.1111/j.1472-8206.2010.00854.x

中图分类号：

R9 [药学];

学科分类号：

100702 [药剂学];

摘要：

Premenopausal women are protected to some extent from cardiovascular and kidney diseases. Because this protection weakens after menopause, sex hormones are believed to play an important role in the pathogenesis of cardiovascular and kidney diseases. The cardiovascular system and the kidneys are regulated by the renin-angiotensin-aldosterone system (RAAS), which in turn, appears to be regulated by sex hormones. In general, oestrogen increases angiotensinogen levels and decreases renin levels, angiotensin-converting enzyme (ACE) activity, AT(1) receptor density, and aldosterone production. Oestrogen also activates counterparts of the RAAS such as natriuretic peptides, AT(2) receptor density, and angiotensinogen (1-7). Progesterone competes with aldosterone for mineralocorticoid receptor. Less is known about androgens, but testosterone seems to increase renin levels and ACE activity. These effects of sex hormones on the RAAS can explain at least some of the gender differences in cardiovascular and kidney diseases.

引用

页码：687 / 698

页数：12

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