Oelkers W K
Department of Medicine, Klinikum Benjamin Franklin (Steglitz), Freie Universität Berlin, Germany.
Steroids. 1996 Apr;61(4):166-71. doi: 10.1016/0039-128x(96)00007-4.
Endogenous 17 beta-estradiol (E2) and low parenteral doses of exogenous E2 are vasodilators. High dose estrogens, especially ethinylestradiol (EE) and mestranol, stimulate the synthesis of hepatic proteins including coagulation factors, sex hormone binding globulin, and angiotensinogen (Aogen). In the steady state, high plasma levels of Aogen produce only a very small increase of angiotensin II (AII) and plasma renin activity, because AII inhibits the secretion of renin and lowers plasma renin concentration. However, the increase in AII is sufficient for a slight reduction in renal blood flow and a slight increase in exchangeable sodium and blood pressure; in susceptible women, blood pressure may rise considerably. Effects of estrogens on the brain may also be involved in blood pressure changes. Endogenous progesterone is a mineralocorticoid receptor antagonist. Endogenous or exogenous progesterone leads to sodium loss and a compensatory increase in renin secretion, plasma renin activity, AII, and plasma aldosterone, e.g. in the second half of the menstrual cycle. Synthetic progestogens are commonly devoid of the mineralocorticoid receptor antagonistic effect of progesterone, and some are weak estrogen receptor agonists. Combined use of EE and synthetic progestogens may therefore enhance estrogen effects on body sodium and blood pressure. A new progestogen (Drospirenone) with an antimineralocorticoid effect like that of progesterone is described that slightly lowers body weight and blood pressure in a contraceptive formulation together with EE. An almost ideal oral contraceptive would be progestogen like Drospirenone together with a low dose natural estrogen that does not stimulate Aogen synthesis. Since most oral formulations for postmenopausal estrogen replacement also stimulate hepatic protein synthesis (including Aogen) to some extent, the transdermal route of E2 application for contraceptive purposes should also be investigated, since it has reduced potential for undesirable side effects.
内源性17β-雌二醇(E2)和低剂量肠外给予的外源性E2具有血管舒张作用。高剂量雌激素,尤其是炔雌醇(EE)和炔诺醇,可刺激肝脏蛋白质的合成,包括凝血因子、性激素结合球蛋白和血管紧张素原(Aogen)。在稳态时,高血浆水平的Aogen只会使血管紧张素II(AII)和血浆肾素活性有非常小的升高,因为AII会抑制肾素分泌并降低血浆肾素浓度。然而,AII的升高足以使肾血流量略有减少,可交换钠和血压略有升高;在易感女性中,血压可能会显著升高。雌激素对大脑的作用也可能与血压变化有关。内源性孕酮是一种盐皮质激素受体拮抗剂。内源性或外源性孕酮会导致钠流失,并使肾素分泌、血浆肾素活性、AII和血浆醛固酮代偿性增加,例如在月经周期的后半期。合成孕激素通常缺乏孕酮的盐皮质激素受体拮抗作用,有些还是弱雌激素受体激动剂。因此,EE与合成孕激素联合使用可能会增强雌激素对机体钠和血压的影响。有一种新的具有类似孕酮抗盐皮质激素作用的孕激素(屈螺酮),在与EE的避孕制剂中,它能轻微降低体重和血压。一种近乎理想的口服避孕药应该是类似屈螺酮的孕激素与不刺激Aogen合成的低剂量天然雌激素。由于大多数绝经后雌激素替代的口服制剂也会在一定程度上刺激肝脏蛋白质合成(包括Aogen),因此也应研究经皮应用E2用于避孕的途径,因为它产生不良副作用的可能性较小。