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性别与肾素-血管紧张素-醛固酮系统。

Gender and the renin-angiotensin-aldosterone system.

机构信息

Division of Cardiology, The Jikei University School of Medicine, 3-25-8 Nishi-shimbashi, Minato-ku, Tokyo 105-8461, Japan.

出版信息

Fundam Clin Pharmacol. 2010 Dec;24(6):687-98. doi: 10.1111/j.1472-8206.2010.00854.x.

Abstract

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.

摘要

绝经前女性在一定程度上受到保护,免受心血管和肾脏疾病的侵害。由于这种保护作用在绝经后减弱,因此性激素被认为在心血管和肾脏疾病的发病机制中起重要作用。肾素-血管紧张素-醛固酮系统 (RAAS) 调节心血管系统和肾脏,而 RAAS 似乎又受到性激素的调节。一般来说,雌激素会增加血管紧张素原水平并降低肾素水平、血管紧张素转换酶 (ACE) 活性、AT(1)受体密度和醛固酮生成。雌激素还会激活 RAAS 的类似物,如利钠肽、AT(2)受体密度和血管紧张素原 (1-7)。孕激素与醛固酮竞争盐皮质激素受体。关于雄激素的了解较少,但似乎睾酮会增加肾素水平和 ACE 活性。性激素对 RAAS 的这些影响至少可以解释心血管和肾脏疾病中一些性别差异的原因。

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