The role of the renin-angiotensin-aldosterone system in cardiovascular homeostasis in normal human subjects.
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, which blocked the generation of angiotensin II, sodium replete subjects were able to compensate for an upright tilt, despite the absence of angiotensin II, 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 II is the primary stimulus to aldosterone secretion in response to both sodium depletion and to posture.
D000328:Adult; D000450:Aldosterone / Q000378:metabolism / Q000502:physiology*; D000804:Angiotensin II / Q000502:physiology*; D000806:Angiotensin-Converting Enzyme Inhibitors; D001794:Blood Pressure; D001920:Bradykinin / Q000097:blood; D004232:Diuretics; D005246:Feedback; D005260:Female; D006706:Homeostasis; D006801:Humans; D008297:Male; D011187:Posture; D012083:Renin / Q000502:physiology*; D012964:Sodium / Q000172:deficiency; D013722:Teprotide
D000806:Angiotensin-Converting Enzyme Inhibitors; D004232:Diuretics; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D013722:Teprotide; D012083:Renin; D001920:Bradykinin