Potentiation of bradykinin by captopril during suppression of prostacyclin synthesis.
The effect of captopril on blood pressure and on the depressor responses to intravenously administered bradykinin was examined in anesthetized normotensive rats during inhibition of prostaglandin synthesis. The hypotensive action of captopril persisted after treatment with indomethacin in doses that markedly suppressed urinary excretion of the prostacyclin metabolite 6-keto prostaglandin F1 alpha. Captopril markedly potentiated the vasodepressor responses to intravenous bradykinin given by bolus injection or continuous infusion. Neither the magnitude nor the duration of the blood pressure fall were affected by treatment with indomethacin. It is concluded that in the anesthetized rat the hypotensive action of captopril and its augmentation of the depressor response to bradykinin is independent of prostacyclin synthesis.
D015121:6-Ketoprostaglandin F1 alpha / Q000652:urine; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001920:Bradykinin / Q000494:pharmacology*; D002216:Captopril / Q000494:pharmacology*; D004357:Drug Synergism; D011464:Epoprostenol / Q000502:physiology*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011392:Proline / Q000031:analogs & derivatives*; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D011453:Prostaglandins / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D014664:Vasodilation / Q000187:drug effects
D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D015121:6-Ketoprostaglandin F1 alpha; D011392:Proline; D002216:Captopril; D011464:Epoprostenol; D001920:Bradykinin; D007213:Indomethacin