Effect of indomethacin on antihypertensive action of captopril in hypertensive patients.
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 thirteen patients with essential hypertension, during three experimental periods: on a normal-sodium diet (150 mEq per day), on a low-sodium diet (30 mEq per day), and on a low-sodium diet following with indomethacin 150 mg daily for three days. During the normal-sodium and low-sodium periods, BP was significantly decreased after the administration of captopril, accompanied by a significant increase in urinary PGE2 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 prostaglandin, in addition to a reduction in circulating angiotensin II. Moreover, 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. These results suggest that the prostaglandin systems may play an important role in vasodepressor action of captopril in patients with essential hypertension, especially in a low-renin group.
D000328:Adult; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000627:therapeutic use*; D004039:Diet, Sodium-Restricted; D015232:Dinoprostone; D006801:Humans; D006973:Hypertension / Q000503:physiopathology* / Q000628:therapy; D007213:Indomethacin; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D011392:Proline / Q000031:analogs & derivatives*; D011458:Prostaglandins E / Q000652:urine; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism
D011458:Prostaglandins E; D011392:Proline; D002216:Captopril; D012964:Sodium; D012083:Renin; D015232:Dinoprostone; D007213:Indomethacin