[Mechanisms of coronary circulation regulation]

Metabolic-induced vasodilation which occurs after sympathetic stimulation of the heart and which results in an increased coronary flow is opposed by an alpha 2-receptor mediated vasoconstriction. Under pathophysiological conditions, when coronary vascular reserve is exhausted (e.g. distal to severe coronary stenosis), alpha 2-receptor induced vasoconstriction can critically limit O2-supply. The identity of vasodilatory metabolic products liberated by the heart is still a matter of debate. Of the several factors proposed (including H+, K+, PO2, PCO2, prostaglandins, adenosine) adenosine is the only metabolite released in dilating quantities into the coronary circulation. This compound is a breakdown product of cardiac adenine nucleotides and acts via specific membrane receptors which mediate activation of the adenylate cyclase system. The major stimulus leading to enhanced adenosine production is a disequilibrium between O2-supply and O2-demand. Besides the cardiac myocyte the coronary endothelium can produce and release adenosine. An intact endothelium is obligatory for the dilatory effects of several vasoactive hormones. The relevance of a myoendothelial mechanism for coronary blood flow regulation, however, remains to be elucidated.