Neural control of vasomotor tone of large coronary arteries.

In man, the occurrence of constrictions of large coronary arteries accompanied by transient myocardial ischemia is now well established. However, the role of neural factors involved in such coronary artery spasms is still a matter of conjecture. A consistent reduction (9 +/- 2%) of the diameter of the large coronary arteries can be obtained in the conscious dog with alpha-adrenergic receptor stimulation with methoxamine in spite of the concomitant pressor rise (65 +/- 5%). Smaller reductions in coronary diameter can be obtained with electrical efferent sympathetic stimulation in anesthetized dogs. The diameter of a conduit artery such as the aorta can be reduced (5%) by reflex increases in sympathetic efferent activity: therefore it is not unlikely that similar neural influences might be exerted on the coronary tree as well. In normal life, stressful situations, such as emotion or exercise, will be accompanied by a drastic increase in sympathetic drive to the heart, together with a marked increase in coronary flow. The latter will induce an endothelial mediated vasodilation; however the net effect on coronary size of these two potentially opposite mechanisms is as yet unexplored. In the laboratory, intracoronary bradykinin and regional myocardial ischemia initiate a reflex increase in sympathetic activity to the heart; in the clinics acute myocardial ischemia can be accompanied by signs of sympathetic overactivity. The extent to which such increases in sympathetic activity, could play a role in the control of coronary tone and hence in the pathophysiology of coronary artery disease, is still under investigation.