Abstract
An endothelin (ET)-converting enzyme inhibitor phosphoramidon (10 μM), an ETAB-receptor antagonist bosentan (10 μM) and an ETA-receptor antagonist BQ-123 (1 μM) potentiated endothelium-dependent relaxation of bovine coronary arteries in response to bradykinin (BK) at femtomolar to picomolar concentrations, but not at nanomolar concentrations. BQ-788 (3 μM), an ETB-receptor antagonist, showed no significant effects on fM – nM BK-induced relaxation. These results suggest that the endothelium-dependent relaxation of isolated bovine coronary arteries induced by very low concentrations of BK is partly regulated by a complex mechanism involving the ETA-receptor antagonism.
