Circulation, Vol 53, 400-405, Copyright © 1976 by American Heart Association
J Sancho, R Re, J Burton, AC Barger and E Haber
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.
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The role of the renin-angiotensin-aldosterone system in cardiovascular homeostasis in normal human subjects
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