Prostacyclin mediates the potentiated hypotensive effect of bradykinin following captopril treatment.
The effect of angiotensin-converting enzyme inhibition by captopril on the release of a prostacyclin-like substance by bradykinin, angiotensin I and angiotensin II was studied by means of the blood-bathed bioassay technique of Vane. Administration of captopril abolished the release of prostacyclin-like substance induced by angiotensin I, potentiated the release provoked by bradykinin and did not alter that due to angiotensin II. Potentiation of the bradykinin-induced renal vasodilatation with captopril could be completely reversed by indomethacin, which also abolished the kinin-induced release of prostacyclin-like substance. Potentiation of the bradykinin-induced hypotension was markedly attenuated but not completely reversed by cyclo-oxygenase inhibition. It is suggested that following converting inhibition increased production of prostacyclin by elevated kinin levels may contribute to the antihypertensive action of angiotensin-converting enzyme inhibitors.
D000803:Angiotensin I / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001920:Bradykinin / Q000494:pharmacology*; D002216:Captopril / Q000494:pharmacology*; D004285:Dogs; D011464:Epoprostenol / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply; D008297:Male; D011392:Proline / Q000031:analogs & derivatives*; D011453:Prostaglandins / Q000502:physiology*; D012039:Regional Blood Flow / Q000187:drug effects
D011453:Prostaglandins; D000804:Angiotensin II; D000803:Angiotensin I; D011392:Proline; D002216:Captopril; D011464:Epoprostenol; D001920:Bradykinin; D007213:Indomethacin