Mechanism and modification of bradykinin-induced coronary vasodilation.
Abstract
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.
- Publication:
-
Proceedings of the National Academy of Science
- Pub Date:
- June 1975
- DOI:
- 10.1073/pnas.72.6.2060
- Bibcode:
- 1975PNAS...72.2060N