Endothelium dependent vasomotor responses to endogenous agonists are potentiated following ACE inhibition by a bradykinin dependent mechanism

Abstract

In the coronary vasculature of the dog, ACE inhibitors enhance vasomotor responses to endothelium dependent agonists by facilitating the release of both NO and PGI2, a mechanism which is coupled to endogenously formed bradykinin. ACE inhibitors may thus mediate their effects in vivo partly by increasing the capacity of the endothelium to release autacoids.