Myocardial beta-adrenoceptors mediate physiological effects of the agonists noradrenaline und adrenaline and stimulant effects of related amines and beta-blockers. At least 2 beta-adrenoceptor subtypes appear to contribute to the mediation of physiological effects. beta-adrenoceptor subtypes have recently been found with selective beta-blockers and nonphysiological agonists in several heart regions. However, no evidence has yet been reported that the affinity of a physiological agonist for cardiac beta-adrenoceptor subtypes differs. The possibility is discussed that an agonist may cause greater conformational change of one subtype than of another while binding to the same extent to both beta-adrenoceptor populations. The affinity of catecholamines for beta-adrenoceptors is low. Marked positive inotropic and chronotropic effects occur with catecholamine concentrations causing low beta-adrenoceptor occupancy and barely suprathreshold stimulation of the adenylyl cyclase. The large beta-adrenoceptor reserve and adenylyl cyclase reserve enable the regulation of the sinoatrial pacemaker activity and of ventricular and atrial contractility. Thus exposure to high catecholamine concentrations causes a pronounced decrease of Vmax for the adenylyl cyclase with a concurrent decrease in inotropic and chronotropic potencies, but without decreasing maximum inotropic and chronotropic effects of catecholamines. Data from isolated human myocardium suggest that the intropic potency of catecholamines is lower and the adenylyl cyclase reserve smaller than in other species. Pindolol, its derivatives, and some other partial agonists only cause positive chronotropic effects at concentrations considerably higher than those required to half-saturate cardiac beta-receptors.