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The regulation of the renin-angiotensin-aldosterone system by sex hormones provides a physiological explanation for gender differences in cardiovascular and kidney disease susceptibility.
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.
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Komukai et al. (2010) studied this question.
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