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

Journal of EndocrinologyPublished 1 December 1981
Jan A. Staessen, Paul Lijnen, R. Fagard, L J Verschueren, A. Amery
Citations335
SJR quartileQ1
SJR score1.19
SNIP1.03

TL;DR

The plasma concentration of aldosterone was followed in seven hypertensive patients before and during long-term angiotensin II suppression with the orally active ang Elliotensin-I-converting-enzyme inhibitor, captopril to find the mechanism responsible for the late rise of the plasma concentration.

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 less than 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.

Keywords

MedicineBiochemistry, Genetics and Molecular Biology