Postjunctional alpha-adrenoceptor subtypes in isolated and perfused canine epicardial coronary arteries

In isolated and perfused canine coronary arteries pretreated with propranolol (5 x 10(-6) M), effects of bunazosin (E 643, a selective alpha 1-antagonist) and DG 5128 (a selective alpha 2-antagonist) on vasoconstrictor responses to phenylephrine, xylazine, clonidine, and norepinephrine (NE) were examined. A stainless steel cannula was inserted into the coronary artery segment (1.1-2.4 mm OD, 1.5 cm long) and perfused with Krebs-Henseleit solution at a constant flow rate. The perfusion pressures were 60-110 mm Hg. Acetylcholine readily caused a vasodilation in used arterial preparations. Phenylephrine produced a strong vasoconstriction in a dose-dependent manner, but xylazine and clonidine induced slight vasoconstrictions and a vasodilation followed by a slight vasoconstriction in large doses. Phenylephrine-induced vasoconstrictions were dose-dependently attenuated by bunazosin but not by DG 5128. Neither bunazosin nor DG 5128 blocked the vascular responses to clonidine and xylazine. NE produced a slight vasoconstriction in the presence of prazosin (10(-6) M), and DG 5128 did not influence that vasoconstriction. Diltiazem significantly suppressed KCl-induced vasoconstriction, but bunazosin did not. Removal of endothelium by 1 mg of saponin significantly attenuated acetylcholine (ACh)-induced vasodilation, but did not suppress clonidine-induced vasodilation. It is suggested that only alpha 1-adrenoceptors are involved in the vasoconstrictions induced by the adrenergic agonists in canine epicardial coronary arteries and that the vascular responses to clonidine and xylazine may be direct actions.