Regulation of cardiac sarcolemmal Na+/H+ exchanger activity: potential pathophysiological significance of endogenous mediators and oxidant stress.

摘要: The cardiac sarcolemmal Na+/H+ exchanger (NHE) extrudes one H+ in exchange for Na+ entering the myocyte, utilizing its driving force inwardly directed gradient maintained by Na+, K+-ATPase. is quiescent at physiological values of intracellular pH but becomes activated response to acidosis. Recent evidence suggests that a variety extracellular signals (e.g., adrenergic agonists, thrombin, endothelin, and oxidant stress) also modulate NHE activity altering sensitivity H+. Because believed be an important determinant extent myocardial injury during ischemia reperfusion, regulation factors are associated with likely pathophysiological importance.