Nitric oxide and prostacyclin mediate coronary shear force-induced alterations in cardiac electrophysiology

Abstract

Previous studies have shown that an increase in coronary flow or shear force enhances the oxygen consumption and contractility of myocardium (the “Gregg effect”). Recent studies have indicated that an increase in coronary shear force also affects atrioventricular conduction and ventricular repolarization. The mechanisms of “Gregg effect” and the shear force-induced alterations in cardiac electrophysiology are unclear. It has been proposed that the distension of the coronary arteries and the stretch of the surrounding myocytes may play a key role but this is not supported by the latest studies. Intracoronary perfusion increases coronary endothelial synthesis of nitric oxide and prostacyclin. Emerging evidence has indicated that both nitric oxide and prostacyclin prolong the action potential duration or effective refractory period in the in vitro and in vivo animal heart. We therefore hypothesized that shear force-induced alterations in cardiac function and electrophysiology are largely attributed to the enhanced endothelial release of nitric oxide and prostacyclin.