[Role of prostaglandins in the antihypertensive effect of the converting enzyme inhibitor, enalapril].

Angiotensin converting enzyme (ACE) generates angiotensin II and is also capable of degrading bradykinin into inactive peptides. It has been suggested that the effects of ACE inhibitors are partially mediated by increased prostaglandin synthesis induced by a simultaneous rise in bradykinin. Captopril increases PG excretion and indomethacin (INDO) attenuates its effects. Enalapril is a long acting ACE inhibitor, and its molecule does not have the sulphydryl group present in captopril. In order to evaluate the participations of PG in a the ENA effects of enalapril (ENA) on arterial pressure (AP), plasma renin activity (PRA), plasma aldosterone (ALDO) and renal hemodynamics (RH) in essential hypertension (EHT), we compared the effects of ENA alone and associated with INDO. Nine EHT patients received on different occasions: ENA 10 mg, INDO 25 mg and ENA-INDO. Arterial pressure, PGE2, ALDO, PRA, RH and plasma and urinary ENA as enalaprylate were measured after each treatment. Maximal ENA absorption occurred after 4 hours, however it was still detectable after 72 hr. ENA decreased AP after 6 hr in spite of unchanged PGE2 excretion; PRA did not change and ALDO decreased transiently. INDO delayed ENA absorption, slightly attenuated the fall in AP and suppressed PGE2 excretion when given with ENA. INDO alone suppressed PGE2 and did not alter AP. No significant changes occurred in RH with the treatments. Our results suggest that the antihypertensive effect of ENA is independent of PG, and that the slight attenuation induced by INDO may be attributed to a delay in intestinal absorption. In EHT patients under normovolemic conditions, renal function is not altered by ACE inhibition.