The pharmacologic profile of the novel .beta.-adrenoceptor antagonist/vasodilator, carvedilol, has been investigated in vitro. Carvedilol produced competitive antagonism of the .beta.1-adrenoceptor mediated positive chronotorpic response to isoproterenol in guinea pig atria, and the .beta.2-adrenoceptor mediated relaxation to isoproterenol in carbachol (1 .mu.mol/l) precontacted guinea pig trachea, with a dissociation constant (KB) for .beta.1-adrenoceptors of 0.8 nmol/l and .beta.2-adrenoceptors of 1.3 nmol/l. At slightly higher concentrations, carvedilol produced competitive inhibition of the .alpha.1-adrenoceptor mediated contractile response the norepinephrine in rabbit aorta with a KB of 11 nmol/l. Carvedilol had no significant effect on the contractile responses to angiotensin II in rabbit aorta at concentrations up to 10 .mu.mol/l, thus demonstrating the lack of nonspecific vasodilator action in arteries. In canine saphenous vein., carvedilol produced noncompetitive blockade of .alpha.2-adrenoceptor mediated vasoconstruction, indicative of some additional activity. In estrogen-primed rat uterus precontracted by depolarization with KCl (70 mmol/l), carvedilol produced concentration-dependent relaxation (IC50 of 7.6 .mu.mol/l), consistent with the notion that carvedilol may be a calcium channel antagonist. Support for this hypothesis was obtained in KCl (70 mmol/l) depolarized rabbit aorta where carvedilol (10 .mu.mol/l) produced a 10-fold parallel rightward shift in the concentration-response curve to calcium chloride. These studies demonstrate that carvedilol is a potent .beta.1-, .beta.2- and .alpha.1-adrenoceptor antagonist, and a moderately potent calcium channel antagonist. These multiple activities of carvedilol may contribute to the antihypertensive activity of the compound.