In order to study the regulation of human cardiac and vascular beta-adrenoceptors as induced by beta-adrenoceptor antagonism we determined beta-adrenoceptor density and subtype distribution in right atria, saphenous veins and lymphocytes from 60 patients undergoing coronary artery bypass grafting; 42 of these patients were chronically treated with different beta-adrenoceptor antagonists [without intrinsic sympathomimetic activity: propranolol, sotalol (non-selective); metoprolol, atenolol (beta 1-selective); with intrinsic sympathomimetic activity: pindolol (non-selective)] and 18 patients not treated with beta-adrenoceptor antagonists were taken as controls. In the right atria (70% beta 1-, 30% beta 2-adrenoceptors) of all groups except the pindolol group, total beta-adrenoceptor density was higher than in controls. A more detailed analysis revealed that all beta-adrenoceptor antagonists increased right atrial beta 1-adrenoceptor density, but right atrial beta 2-adrenoceptor density was increased only in the sotalol/propranolol group, remaining unchanged in the metoprolol and atenolol groups, and was decreased in the pindolol group. Similarly, in saphenous veins and circulating lymphocytes (in both, the beta-adrenoceptors were almost exclusively beta 2-adrenoceptors), only propranolol/sotalol increased the beta 2-adrenoceptor density, while metoprolol or atenolol did not affect it. Moreover, in the pindolol group lymphocyte beta 2-adrenoceptor density was decreased. It is concluded that in man all beta-adrenoceptor antagonists without intrinsic sympathomimetic activity increase cardiac and vascular beta-adrenoceptor density, but in a subtype-selective manner. Accordingly, pindolol can be subclassified as a partial beta 2-adrenoceptor agonist.