The regulatory role of the post ulcorner1-and ulcorner2-adrenoceptors on cardiac function, particularly in coronary flow rate, was investigated in the isolated rat heart treated with 10-6 M propranolol. When introduced into the left atrium of the heart, phenylephrine[10-7-10-2 M] decreased coronary flow rate and increased mean coronary resistance in a dose related fashion, but did not affect heart rate. Methoxamine also elicited the increment of coronary resistance and the decrement of coronary flow rate, though the effects of methoxamine were weaker than those by phenylephrine. The effect of phenylephrine was inhibited by 1ulcornerM prazosin and shifting the dose-response curve to the right. The effects of clonidine, a selective ulcorner2-adrenoceptor agonist, were studied in the heart taken from reserpinized rats. Clonidine increased coronary resistance, decreased heart rate and coronary flow rate with a dose-dependent manner. These effects were abolished by 10-6 M yohimbine, a selective ulcorner2-antagonist, and were not affected by 10-6M prazosin. Clonidine also decreased coronary flow and increased mean coronary resistance in electric paced heart. These effects were inhibited by rawoulscine, a selective ca-antagonist. These results indicate that the stimulation of both post ulcorner1-and ulcorner2-adrenoceptor causes coronary vasoconstiction. And it is inferred that this model of sympathomimetics-induced coronary vasospasm may provide a useful tool for investigating spasmolytic agents which are of benefit in the treatment of variant angina.