In patients with chronic heart failure, cardiac beta-adrenoceptor function is decreased, and this decrease is related to the degree of heart failure. Under these conditions, treatment with beta-adrenoceptor agonists seems to be of limited value as it might further down-regulate cardiac beta-adrenoceptors, resulting, finally, in a loss of therapeutic efficacy. However, beta-adrenoceptor antagonists might have beneficial effects, because they can protect the myocardium from the deleterious effects of elevated endogenous catecholamines and can, simultaneously, restore the previously down-regulated beta-adrenoceptor function. Stimulation of cardiac alpha-adrenoceptors, however, seems not to be of any therapeutic value in patients with chronic heart failure, because a) the number of alpha-adrenoceptors in the human heart is very low and its function is not completely understood, and b) no alpha-adrenoceptor agonist is presently available that selectively stimulates cardiac alpha-adrenoceptors without concomitantly activating vascular alpha-adrenoceptors. In acute myocardial ischemia, cardiac beta-adrenoceptors increase; this increase is--at least in early acute myocardial ischemia--accompanied by an increased beta-adrenoceptor functional responsiveness; thus, under these conditions, beta-adrenoceptor agonists again might not be of clinical value, while beta-adrenoceptor antagonists may exert beneficial effects, because they can block (over)activation of the sensitized beta-adrenoceptors by elevated endogenous catecholamines.