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.
|Number of pages||4|
|Journal||Proceedings of the National Academy of Sciences of the United States of America|
|State||Published - 1975|