The Role of the Renin‐Angiotensin‐Aldosterone System in Cardiovascular Homeostasis in Normal Human Subjects
The Role of the Renin‐Angiotensin‐Aldosterone System in Cardiovascular Homeostasis in Normal Human Subjects
复制标题
肾素-血管紧张素-醛固酮系统在正常人体心血管稳态中的作用
DOI：
10.1161/01.cir.53.3.400
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发表时间：
1976
期刊：
影响因子：
37.8
通讯作者：
E. Haber
中科院分区：
文献类型：
--
作者：
J. Sancho;R. Re;J. Burton;A. Barger;E. Haber
为了检查血管紧张素 II 在维持人体血压和控制醛固酮分泌方面的作用，在静脉输注血管紧张素转换酶抑制剂 (CEI) 之前和之后，在倾斜桌上对 8 名正常受试者进行了钠充足和钠耗尽状态的研究。在钠充足或钠耗尽状态下，直立倾斜会导致心率增加和脉压变窄。钠充足或钠耗尽的受试者均未晕倒。倾斜伴随着血浆肾素活性的升高以及血浆醛固酮浓度的相关升高。当施用转化酶抑制剂时，其阻断了血管紧张素II的产生，尽管缺乏血管紧张素11，钠充足的受试者仍能够补偿直立倾斜，与对照状态相比，没有显着的血流动力学变化。在钠耗尽的受试者中，施用转化酶抑制剂后，收缩压和舒张压急剧下降，并伴有心率显着上升。除一名钠耗尽的受试者外，所有受试者均在七分钟内晕倒。在钠充足和钠耗尽的受试者中，血浆醛固酮浓度和血浆肾素活性均随着倾斜而升高。给予转化酶抑制剂后，血浆醛固酮未能随着血浆肾素活性的升高而升高。在仰卧位受试者中，给予转化酶抑制剂后，血浆肾素活性上升，但血浆醛固酮浓度下降。在钠耗尽的受试者中，施用CEI后，醛固酮下降到显着低于仰卧对照组的水平，并且与仰卧钠充足的受试者没有不同的水平。这些结果表明，血管紧张素II对于钠缺乏个体的血压维持至关重要，血管紧张素II对肾素分泌发挥直接反馈控制，并且血管紧张素II是响应于钠缺乏和姿势两者的醛固酮分泌的主要刺激物。
To examine the role of angiotensin II in the maintenance of blood pressure and the control of aldosterone secretion in man, eight normal subjects were studied on a tilt table in sodium replete and sodium depleted states prior to and subsequent to the intravenous infusion of an angiotensin converting enzyme inhibitor (CEI). In both the sodium replete or sodium depleted state, upright tilting resulted in an increase in heart rate and a narrowing of pulse pressure. None of the sodium replete or depleted subjects fainted. Tilting was accompanied by a rise in plasma renin activity with an associated rise in plasma aldosterone concentration. When converting enzyme inhibitor was administered, wbich blocked the generation of angiotensin II, sodium replete subjects were able to compensate for an upright tilt, despite the absence of angiotensin 11, without significant hemodynamic change when compared to control state. In sodium depleted subjects, after the administration of converting enzyme inhibitor, there was a sharp and significant decrease in systolic and diastolic blood pressure associated with a significant rise in heart rate. All but one sodium depleted subject fainted within seven minutes. Both plasma aldosterone concentration and plasma renin activity rose on tilting in both sodium replete and sodium depleted subjects. After the administration of converting enzyme inhibitor, plasma aldosterone failed to rise in association with a rise in plasma renin activity. In supine subjects, after the administration of converting enzyme inhibitor, plasma renin activity rose but plasma aldosterone concentration fell. In sodium depleted subjects, after the administration of CEI, aldosterone fell to a level significantly lower than that in supine controls and to a level no different from the supine sodium replete subject. These results indicate that angiotensin II is essential for blood pressure maintenance in sodium depleted individuals, that angiotensin II exerts a direct feedback control on renin secretion, and that angiotensin It is the primary stimulus to aldosterone secretion in response to both sodium depletion and to postur.