Neural Control of Coronary Blood Flow

Abstract

Parasympathetic control of coronary blood flow has been extensively studied in dogs, and a clear vasodilator effect not dependent on changes in myocardial metabolism was observed. Parasympathetic vasodilatation is mediated via nitric oxide (EDRF) and is activated during carotid baroreceptor and chemoreceptor reflexes. Intracoronary infusions of acetylcholine in humans results in increased coronary blood flow and epicardial coronary artery dilatation except in atherosclerotic epicardial coronary vessels, which show a paradoxical vasoconstriction. Sympathetic α-adrenoceptor-mediated coronary vasoconstriction has been repeatedly demonstrated whenever there is adrenergic activation of the heart, as during exercise or a carotid sinus baroreceptor reflex in dogs or during a cold pressor reflex in humans. Recent evidence indicates that there is a beneficial effect of this paradoxical vasoconstrictor influence in that it helps preserve flow to the vulnerable inner layer of the left ventricle, but only when both heart rate and coronary flow are high. β-Adrenoceptor-mediated coronary vasodilatation also occurs during adrenergic activation of the heart. The dominant site for β-vasodilatation is in small arterioles, while the dominant site for α-vasoconstriction is in microvessels larger than ∼100 µm diameter. The β-adrenoceptor coronary vasodilatation is an example of feedforward open-loop control that complements the closed-loop negative feedback control by local metabolic factors. The combined feedback and feedforward control mechanism has the advantage of an excellent match between coronary blood flow and myocardial oxygen consumption with a rapid response time but without the instability inherent in high gain feedback systems.