Carvedilol is a combined alpha(1)- and beta-adrenoceptor antagonist. We investigated the ability of carvedilol to antagonize functional effects mediated through myocardial alpha(1)-adrenoceptors in failing vs. non-failing (sham-operated) control hearts and compared such antagonisms to those of myocardial beta-adrenoceptors. Congestive heart failure was induced in Wistar rats by coronary artery ligation. Papillary muscles experiments were performed. Carvedilol antagonized inotropic effects mediated through myocardial alpha(1)-adrenoceptors with similar potencies in failing (pK(i)=7.7 (95%, CI; 7.4-8.0)) and sham-operated hearts (pK(i)=7.9 (95%, CI; 7.6-8.1)). The potency for the alpha(1)-adrenoceptors was 10-30-fold lower than that for the beta-adrenoceptors. In failing hearts, the alpha(1)-adrenoceptor mediated response was similar in size to the attenuated beta-adrenoceptor mediated inotropic response. The beta-adrenoceptor mediated lusitropic effects were not, however, attenuated in failing compared to sham-operated hearts. A low degree of alpha(1)-adrenoceptor blockade in the myocardium may contribute to the beneficial effects of carvedilol in heart failure.