Estrogen and hypertension
Estrogen and hypertension
复制标题
DOI：
10.1007/s11906-006-0080-1
复制
发表时间：
2006-10-01
影响因子：
5.6
通讯作者：
Vongpatanasin, Wanpen
中科院分区：
文献类型：
--
作者：
Ashraf, Muhammad S.;Vongpatanasin, Wanpen
绝经期伴随着女性高血压患病率的急剧上升，提示内源性雌二醇对血压（BP）具有保护作用。动物实验和人类临床研究表明，雌激素参与了几种预防高血压的机制，如激活由一氧化氮和前列环素介导的血管扩张途径，抑制由交感神经系统和血管紧张素介导的血管收缩途径。然而，来自最近临床试验的新证据表明，绝经后妇女口服雌激素可使收缩压小幅升高，而不是降低，对舒张压没有任何可检测到的影响。绝经后妇女收缩压选择性升高和绝经前妇女口服避孕药引起的高血压的机制尚不清楚，但这种升高可能与肝脏中雌激素的超生理浓度有关。迄今为止，经皮给药雌激素避免了雌二醇的首过肝脏代谢，似乎对绝经后妇女有小的降血压作用，对高血压妇女可能是一种更安全的选择。
Menopause is accompanied by a dramatic rise in the prevalence of hypertension in women, suggesting a protective role of endogenous estradiol on blood pressure (BP). Both animal experimental and human clinical investigations suggest that estrogen engages several mechanisms that protect against hypertension, such as activation of the vasodilator pathway mediated by nitric oxide and prostacyclin and inhibition of the vasoconstrictor pathway mediated by the sympathetic nervous system and angiotensin. However, emerging evidence from recent clinical trials indicates a small increase, rather than decrease, in systolic BP with oral estrogen administration in postmenopausal women, without any detectable effect on diastolic BP. Mechanisms underlying this selective rise in systolic BP in postmenopausal women and oral contraceptive-induced hypertension in premenopausal women remain unknown, but the rise may be related to supraphysiologic concentration of estrogen in the liver. To date, transdermal delivery of estrogen, which avoids the first-pass hepatic metabolism of estradiol, appears to have a small BP-lowering effect in postmenopausal women and may be a safer alternative in hypertensive women.