Heart Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
J Mol Cell Cardiol. 2013 Aug;61:28-33. doi: 10.1016/j.yjmcc.2013.06.001. Epub 2013 Jun 12.
Sodium-calcium exchange (NCX) is the major calcium (Ca) efflux mechanism of ventricular cardiomyocytes. Consequently the exchanger plays a critical role in the regulation of cellular Ca content and hence contractility. Reductions in Ca efflux by the exchanger, such as those produced by elevated intracellular sodium (Na) in response to cardiac glycosides, raise sarcoplasmic reticulum (SR) Ca stores. The result is an increased Ca transient and cardiac contractility. Enhanced Ca efflux activity by the exchanger, for example during heart failure, may reduce diadic cleft Ca and excitation-contraction (EC) coupling gain. This aggravates the impaired contractility associated with SR Ca ATPase dysfunction and reduced SR Ca load in failing heart muscle. Recent data from our laboratories indicate that NCX can also impact the efficiency of EC coupling and contractility independent of SR Ca load through diadic cleft priming with Ca during the upstroke of the action potential. This article is part of a Special Issue entitled "Na(+) Regulation in Cardiac Myocytes".
钠钙交换(NCX)是心室肌细胞中钙(Ca)外流的主要机制。因此,该交换器在调节细胞内 Ca 含量和收缩性方面起着关键作用。交换器的 Ca 外流减少,例如心脏糖苷类药物引起的细胞内 Na 升高所产生的 Ca 外流减少,会增加肌浆网(SR)Ca 储存。结果是 Ca 瞬间增加和心脏收缩力增强。交换器的 Ca 外流活性增强,例如在心力衰竭期间,可能会降低二联体裂孔 Ca 和兴奋-收缩(EC)偶联增益。这会加剧与 SR Ca ATP 酶功能障碍和衰竭心肌中 SR Ca 负荷减少相关的收缩功能障碍。我们实验室的最新数据表明,NCX 还可以通过动作电位上升过程中二联体裂孔中的 Ca 引发来影响 EC 偶联和收缩力的效率,而与 SR Ca 负荷无关。本文是题为“心肌细胞中的 Na(+)调节”的特刊的一部分。