Coronary blood flow has long been regarded as being regulated primarily by the metabolic demand of the myocardium [1,2]. Experimental and clinical reports [3-9], however, indicate that such coronary regulation can be overridden by the adrenergic drive to the heart. In particular, previous studies in dogs [7,10] demonstrated that carotid sinus hypotension results in a reflex sympathetic a-receptor coronary vasoconstriction, independent of changes in myocardial oxygen metabolism or aortic pressure. Other investigators [4] observed in dogs that stimulation of the carotid sinus nerve can produce a profound coronary vasodilatation mediated by reflex suppression of tonic a-vasoconstrictor tone. Finally, we described in humans a reflex increase of coronary vascular resistance induced by reduction in carotid transmural pressure [11]. While a modulatory role of arterial baroreceptors has been demonstrated, the possible influence exerted by cardiopulmonary receptors on the coronary vascular tone is still debated. It is well known that these receptors affect peripheral vascular tone [12,13]; in addition, Thames [14] has shown reflex withdrawal of renal sympathetic dis-