ORIGINAL ARTICLE: PDF OnlyNakane Tokio; Chiba, ShigetoshiJournal of Cardiovascular Pharmacology: December 1987 - p 651-657 Free Abstract Summary: In isolated and perfused canine coronary arteries pretreated with propranolol (5 x I0−6M), effects of bunazosin (E 643, a selective α1-antagonist) and DG 5128 (a selective α2-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-in-duced 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 (10−6M), and DG 5128 did not influence that vasoconstriction. Diltiazem significantly suppressed KCI-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 α1-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 © Lippincott-Raven Publishers.