Left coronary perfusion pressure was reduced to 50 mm Hg in alpha-chloralose-anesthetized open chest dogs, causing significant reductions in coronary blood flow and left ventricular oxygen consumption (P less than .05). Infusion of the specific alpha-1 adrenergic antagonist prazosin (0.1 mg/min i.c.) during coronary hypotension significantly increased coronary flow and oxygen consumption within 6 to 8 min. These effects of prazosin were not attenuated by beta adrenergic blockade with propranolol. In the absence of propranolol, infusion of the nonspecific alpha adrenergic antagonist phenoxybenzamine (0.37 mg/min i.c.) increased coronary flow and oxygen consumption within 10 to 15 min, and these increases were significantly greater than with prazosin. In the presence of propranolol, phenoxybenzamine caused increases in coronary flow and oxygen consumption that were not different from those caused by prazosin. The results indicate that 1) prazosin increases coronary flow and oxygen delivery by abolition of a coronary constrictor tone mediated by postsynaptic alpha adrenoceptors; 2) the increases in coronary flow and oxygen consumption caused by phenoxybenzamine in the absence of beta adrenergic blockade were due to antagonism of pre- and postsynaptic alpha adrenoceptors; and 3) the increases in coronary flow and oxygen consumption caused by phenoxybenzamine after beta adrenergic blockade were due entirely to antagonism of coronary postsynaptic alpha-1 adrenoceptors.