Regulation of large coronary arteries

Abstract

The majority of studies on the control of coronary artery vasoactivity have examined changes in coronary blood flow and coronary vascular resistance, indices that primarily reflect regulation of small arterioles and precapillary vessels. With the emergence of coronary artery vasospasm as a significant cause of angina pectoris, myocardial infarction, and sudden death, the control of large coronary artery caliber has assumed more significance. It is clear that resistance coronary vessels and large coronary arteries differ in response to both pharmacologic and physiologic stimuli. Vasodilation of large coronary arteries may occur by direct action of agents on the arterial smooth muscle or by the indirect action of receptor occupation, changes in blood flow, or liberation of endothelial factors. These indirect factors appear to contribute also to responses to agents that constrict coronary smooth muscle directly or through the autonomic nervous system. Furthermore, the mechanisms responsible for control of large coronary vessels in the normal circulation are likely to be profoundly different from those in the presence of diseased vessels. For example, several factors associated with coronary artery disease--elevated plasma cholesterol levels, endothelial disruption, atherosclerosis, vascular stenosis, and aggregated platelets--all have important actions on the control of large coronary arteries.