RISE IN PLASMA CONCENTRATION OF ALDOSTERONE DURING LONG-TERM ANGIOTENSIN II SUPPRESSION

TLDR

The mechanism behind the late rise in plasma aldosterone during long‑term angiotensin‑II suppression with captopril is still unknown. The study monitored plasma aldosterone levels in seven hypertensive patients before and during prolonged captopril therapy. After one month of captopril, aldosterone dropped from 74 to 21 pg/ml, then rose to 165 pg/ml over a year while renin activity remained elevated, angiotensin II stayed suppressed, and a sustained hypotensive effect was observed in all patients.

Abstract

The plasma concentration of aldosterone was followed in seven hypertensive patients before and during long-term angiotensin II suppression with the orally active angiotensin-I-converting-enzyme inhibitor, captopril. The plasma concentration of aldosterone decreased initially from 74 to 21 pg/ml ( P < 0·05) after 1 month of administration of captopril. Thereafter the plasma concentration of aldosterone began to rise and after 1 year reached a level of 165 pg/ml. During long-term captopril therapy the plasma renin activity remained increased and the plasma angiotensin II concentration suppressed. The mechanism responsible for the late rise of the plasma concentration of aldosterone during long-term angiotensin II suppression with captopril remains to be elucidated. A sizeable and lasting hypotensive effect was observed in all patients.