Journal of Clinical Endocrinology & Metabolism, Vol 52, 354-358, Copyright © 1981 by Endocrine Society

ARTICLES

Suppression of captopril-induced increase in plasma renin activity by des-Asp1-,Ileu8-angiotensin II in man

T Kono, F Ikeda, F Oseko, H Imura and J Endo

One hundred milligrams of oral captopril (SQ 14225) caused a significant increase in PRA and a significant decrease in plasma aldosterone (PA) in five normal men and five hypertensive patients. Blood pressure (BP) showed no change in the normal men, but it fell significantly in the patients. An iv infusion of 200 ng/kg.min des-Asp1- ,Ileu8-angiotensin II (AIIIA) for 2 h caused a significant decrease in PRA and a slight but significant increase in PA, but caused no change in BP in the normal men. When 100 mg captopril were given orally immediately before the start of the AIIIA infusion, BP showed no change in the normal men, but fell in the patients. However, PRA showed a significant decrease and PA showed a slight but significant increase in both the normal men and the patients, except for one patient with renovascular hypertension who showed a decrease in PA. Thus, this suppression of captopril-induced PRA increase by AIIIA, a derivative of angiotensin II, is not related to BP change, and it suggests that the principal cause of the PRA increase after captopril is a disappearance of endogenous angiotensin II.

This article has been cited by other articles:

				P. Lijnen, V. Petrov, K. Rumilla, and R. Fagard Stimulation of collagen gel contraction by angiotensin II and III in cardiac fibroblasts Journal of Renin-Angiotensin-Aldosterone System, September 1, 2002; 3(3): 160 - 166. [Abstract] [PDF]