The pathophysiological role of sympathetic coronary innervation in myocardial ischemia is not clear, probably due to the complexities of adrenergic vascular control. In the canine coronary bed in vivo under beta-adrenergic blockade, alpha 1- as well as alpha 2-adrenoceptor-mediated constrictions can be elicited with predominance of the former in the epicardial conductance arteries, and of the latter in coronary resistance vessels. However, this distribution of functional responsiveness cannot indicate distribution of receptor density and cannot remain unchanged under differing conditions. First, each of these two classes of alpha-adrenoceptors consists of a mixture of different, interacting subtypes; second, the smooth muscular responsiveness to these two classes of alpha-adrenoceptors is differently modulated by contractile preactivation, by beta 2-blockade, and by the influence of sympathetic cotransmitters; third, alpha-adrenoceptors on endothelial cells and on sympathetic nerve endings can substantially modulate sympathetic coronary constriction. Thus, this neurogenic coronary control possesses a great functional plasticity, which is not yet fully evaluated with the presently available pharmacological tools.