A ROLE FOR THE SARCOLEMMAL NA+/H+ EXCHANGER IN THE SLOW FORCE RESPONSE TO MYOCARDIAL STRETCH

摘要: Although the contractile performance of myocardium is under continuous nervous and hormonal regulation, possesses a number intrinsic, load-dependent mechanisms by which it can adjust cardiac output to meet needs circulation over periods ranging from seconds years. In isolated hearts, an increase in ventricular end-diastolic volume (EDV), produced increased venous return or decreased aortic outflow, leads immediately more powerful contraction via Frank-Starling mechanism (“heterometric autoregulation”1 ), so that increases few beats match return. However, next minutes, there further myocardial performance, such EDV returns toward its original value. This second autoregulatory mechanism, “Anrep effect”2 “homeometric autoregulation,”1 allows given change be achieved with smaller than if effect were only compensatory mechanism. Finally, wall stress maintained, genes are switched on eventually lead cell hypertrophy. Much known about cellular molecular basis initial stages load-induced hypertrophy, but processes responsible for Anrep poorly understood. this issue Circulation Research , Alvarez et al3 suggest novel slow contractility: stretch-induced activation sarcolemmal Na+/H+ exchanger (NHE) local autocrine/paracrine systems involving angiotensin II (Ang II) endothelin-1 (ET-1). Our knowledge involved time-dependent contractility after fiber stretch has come chiefly studies length controlled (for reviews, see References 44 –6). Parmley Chuck7 first show papillary …