Mechanism and modification of bradykinin-induced coronary vasodilation.
In isolated perfused rabbit hearts, bradykinin produced a concentration-dependent decrease in coronary resistance directly associated with biosynthesis and release of prostaglandin-E-like substance. An inhibitor of bradykinin destruction (the nonapeptide SQ-20881) markedly enhanced both the coronary vasodilation and release of prostaglandin-E-like substance produced by cardiac injection of bradykinin. Indomethacin inhibited both the myocardial prostaglandin biosynthesis and the decrease in coronary resistance induced by bradykinin. The demonstration that bradykinin is a potent stimulator of prostaglandin biosynthesis in the heart has implications as to the cause of the afferent cardiovascular reflexes and pain in myocardial infarction and angina pectoris.
D000818:Animals; D001681:Biological Assay; D001920:Bradykinin / Q000494:pharmacology*; D002415:Cats; D002645:Chickens; D003106:Colon / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology; D007583:Jejunum / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D010477:Perfusion; D011453:Prostaglandins / Q000378:metabolism* / Q000494:pharmacology; D011817:Rabbits; D051381:Rats; D012007:Rectum / Q000187:drug effects; D013270:Stomach / Q000187:drug effects; D013722:Teprotide / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology*
D011453:Prostaglandins; D014665:Vasodilator Agents; D013722:Teprotide; D001920:Bradykinin; D007213:Indomethacin