Abstract
An endothelin (ET)-converting enzyme inhibitor phosphoramidon (10 microM), an ET(AB)-receptor antagonist bosentan (10 microM) and an ET(A)-receptor antagonist BQ-123 (1 microM) 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 microM), an ET(B)-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 ET(A)-receptor antagonism.
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