Bravo E L
Adv Nephrol Necker Hosp. 1977;7:105-20.
Four humoral factors have been shown to play important roles in the regulation of aldosterone secretion. These are ACTH, potassium, sodium and angiotensin II. ACTH appears to play little or no role in the maintenance of adrenal zona glomerulosa cells in response to specific stimuli. However, there is evidence to show that physiologic levels of ACTH regulate the minute-to-minute fluctuations of plasma aldosterone. In man and in experimental animals, alterations in potassium balance as well as acute increments in serum potassium can stimulate aldosterone production. The importance of potassium ion in the control of aldosterone secretion can be fully appreciated by the demonstration that aldosterone responses to other stimuli are subnormal in the presence of potassium depletion. Changes in dietary sodium can alter the aldosterone response to a number of acute stimuli. Sodium deprivation enhances aldosterone responses to ACTH infusion, potassium loading and angiotensin II administration. Enhanced conversion of corticosterone to aldosterone (due to sodium depletion) coupled with an acute stimulus acting at an earlier step in aldosterone biosynthesis probably explains the sensitizing effect of dietary sodium restriction. In recent years, indirect evidence has emerged to suggest that the COOH-terminal heptapeptide fragment of angiotensin II may mediate the aldosterone-stimulating activity of the renin-angiotensin system. The evidence has been derived from in vivo and in vitro studies indicating that angiotensin II and the heptapeptide stimulate aldosterone production equally well and that their relative binding potencies to adrenal zona glomerulosa cells are identical. In addition, heptapeptide antagonists are potent and specific inhibitors of angiotensin II-induced aldosterone biosynthesis. However, the data do not preclude the possibility that angiotensin II could stimulate aldosterone production without prior conversion to the heptapeptide.
已证明有四种体液因素在醛固酮分泌调节中起重要作用。这些因素是促肾上腺皮质激素（ACTH）、钾、钠和血管紧张素II。在肾上腺球状带细胞对特定刺激的反应维持方面，ACTH似乎作用很小或不起作用。然而，有证据表明，生理水平的ACTH调节血浆醛固酮的每分钟波动。在人和实验动物中，钾平衡的改变以及血清钾的急性升高可刺激醛固酮的产生。通过证明在钾缺乏情况下醛固酮对其他刺激的反应低于正常水平，可以充分认识到钾离子在醛固酮分泌控制中的重要性。饮食中钠的变化可改变醛固酮对多种急性刺激的反应。缺钠会增强醛固酮对ACTH输注、钾负荷和血管紧张素II给药的反应。（由于缺钠）皮质酮向醛固酮的转化增强，再加上在醛固酮生物合成早期阶段起作用的急性刺激，可能解释了饮食中钠限制的致敏作用。近年来，已出现间接证据表明血管紧张素II的COOH末端七肽片段可能介导肾素-血管紧张素系统的醛固酮刺激活性。该证据来自体内和体外研究，表明血管紧张素II和七肽对醛固酮产生的刺激作用相同，且它们与肾上腺球状带细胞的相对结合能力相同。此外，七肽拮抗剂是血管紧张素II诱导的醛固酮生物合成的强效特异性抑制剂。然而，这些数据并不排除血管紧张素II在不预先转化为七肽的情况下刺激醛固酮产生的可能性。
