Captopril in primary hypertension. Effects related to the renin-angiotensin-aldosterone and kallikrein-kinin systems.

The effects of captopril (SQ 14.225), an orally active inhibitor of angiotensin converting enzyme, were investigated in a dose titration study of primary hypertension. In 32 patients 4 weeks titration with captopril gave a mean blood pressure (BP) reduction of 26/16 mmHg supine and 30/16 mmHg standing. No serious side effects were observed. The BP lowering effect was related to pretreatment plasma renin activity and was less in low renin hypertension (p less than 0.05). Captopril reduced angiotensin II (p less than 0.05), plasma (p less than 0.005) and urinary aldosterone (p less than 0.001) as well as urinary kallikrein excretion (p less than 0.005). Captopril (SQ 14.225) is a competitive inhibitor of peptidyl dipeptide hydrolase, also known as angiotensin converting enzyme (ACE) or kininase II, which converts angiotensin I (A I) into angiotensin II (A II), hydrolyzes des-Asp-angiotensin I to angiotensin III (A III) and inactivates bradykinin (BK) (19). Captopril has potent antihypertensive effects when used in human hypertension (review, 3) especially when the renin-angiotensin-aldosterone system (RAAS) is activated. To further investigate the mode of action and the hypotensive effect of captopril, we measured plasma renin activity (PRA), A II, plasma (PA) and urinary aldosterone excretion (UA) and urinary kallikrein excretion (UK) in 32 patients with established primary (essential) hypertension.