Increase in prostaglandins during converting enzyme inhibition.
1. Because changes in the plasma concentration of angiotensin II and bradykinin appear inadequate to account completely for the hypotensive response to captopril, we measured changes in plasma prostaglandins in response to increasing doses of captopril in nine supine normal male subjects studied on both a high (200 mol/l) and low (10 mol/l) sodium intake. 2. On both the high and low sodium diets, captopril induced significant (P < 0.01) increments in the 13,14-dihydro-15-keto metabolite of the vasodilatory prostaglandin E2, which correlated significantly with the fall in blood pressure (P < 0.0001). 3. No significant changes were noted in the plasma levels of 6-keto-prostaglandins F1 alpha or thromboxane B2, the stable products of prostacyclin and thromboxane A2 respectively.
D000328:Adult; D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D007705:Kinins / Q000097:blood; D008297:Male; D011392:Proline / Q000031:analogs & derivatives*; D011453:Prostaglandins / Q000097:blood*; D011458:Prostaglandins E / Q000097:blood; D012964:Sodium / Q000378:metabolism; D013997:Time Factors
D000806:Angiotensin-Converting Enzyme Inhibitors; D007705:Kinins; D011453:Prostaglandins; D011458:Prostaglandins E; D000804:Angiotensin II; D011392:Proline; D002216:Captopril; D012964:Sodium