Effect of Indomethacin on Antihypertensive Action of Captopril in Hypertensive Patients

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Abstract
To evaluate the role of prostaglandin systems in mediating the response of blood pressure (BP) to the converting enzyme inhibitor, single dose of captopril, 100 mg, was administered orally in 13 patients with essential hypertension, during 3 experimental periods: on a normal Na diet (150 meq/day), on a low-Na diet (30 meq/day), and on a low-Na diet following with indomethacin 150 mg daily for 3 days. During the normal-Na and low-Na periods, BP was significantly decreased after the administration of captopril, accompanied by a significant increase in urinary PGE2 [prostaglandin E2] excretion. With the indomethacin treatment, captopril-induced fall in BP was markedly inhibited, not associated with the apparent increase in urinary PGE2 excretion. The evidence presented suggests that antihypertensive effect of captopril may be due to overproduction of PG, in addition to a reduction in circulating angiotensin II. The indomethacin-inhibiting effect of the fall in BP caused by captopril was more markedly exhibited in the renin-nonresponder subjects than the renin-responder subjects. Apparently the PG systems may play an important role in vasodepressor action of captopril in patients with essential hypertension, especially in a low-renin group.

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