Sympathetic coronary control

Neural components that participate in the regulation of coronary blood flow include the sympathetic nervous system, the parasympathetic nervous system, coronary reflexes, and possibly, central control of coronary blood flow. Within the sympathetic system, stimulation of the stellate ganglion elicits coronary vasodilation, which is associated with tachycardia and enhanced contractility. This indirect coronary vasodilation is secondary to increased MVO2 related to increased heart rate, contractihty, and aortic pressure and occurs following stellate stimulation. The direct effect of the sympathetic system is a 1-mediated vasoconstriction at rest and during exercise. Other receptor types, 2 and have little influence on tone, whereas /32-stimulation produces a modest vasodUatory effect. Although coronary atherosclerosis may decrease blood flow secondary to obstruction, severe coronary atherosclerosis and obstruction also may increase the sensitivity of coronary arteries to the effects of aj-stimulation and vasoconstriction. 

Vasopressin appears to help maintain arterial blood pressure during episodes of severe hypovolemia/hypotension. There is no convincing evidence for a role of vasopressin in essential hypertension. The effects of vasopressin on the heart (reduced cardiac output and heart rate) are largely indirect and result from coronary vasoconstriction, decreased coronary blood flow, and alterations in vagal and sympathetic tone. Some patients with coronary insufficiency experience angina even in response to the relatively small amounts of vasopressin required to control diabetes insipidus, and vasopressin-induced myocardial ischemia has led to severe reactions and even death. 

The cardiac consequences of baroreceptor-mediated activation of the sympathetic nervous system with minoxidil are similar to those with hydralazine there is an increase in heart rate, myocardial contractility, and myocardial consumption. Thus, myocardial ischemia can be induced by minoxidil in patients with coronary artery disease. The cardiac sympathetic responses are attenuated by concurrent administration of a /3 adrenergic blocker. The adrenergically-induced increase in renin secretion also can be ameliorated by a /3 receptor antagonist or an ACE inhibitor, with enhancement of blood pressure control. 

Eckstein, R. W., Stroud, M., Eckel, R., Dowling, C. V. and Pritchard, W. H., Effects of control of cardiac work upon coronary flow and oxygen consumption after sympathetic nerve stimulation. Am. J. Physiol. 163, (1960). 

Our laboratory has recently investigated the reflex effects of carotid sinus hypertension on the coronary circulation (Ito and Feigl, 1984a). The carotid sinuses were vascularly isolated and perfused with a servo controlled pressure pump. The aortic depressor nerves were cut bilaterally to prevent aortic arch baroreceptor reflexes from buffering carotid sinus reflexes. The left main coronary artery was perfused at constant pressure, and the ventricles were paced at a constant rate following the production of heart block in a closed-chest preparation. Aortic pressure was stabilized with a pressure reservoir and propranolol was administered to block reflex sympathetic effects to the myocardium. Step increases in carotid sinus pressure resulted in graded reflex coronary vasodilation accompanied by increases in coronary sinus oxygen tension. Atropine administration demonstrated that the major portion of the reflex vasodilation was due to parasympathetic activation. These results indicate that parasympathetic coronary vasodilation is part of the carotid sinus baroreceptor reflex. 

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