Leblanc N, Hume J R
Department of Physiology, University of Nevada School of Medicine, Reno 89557-0046.
Science. 1990 Apr 20;248(4953):372-6. doi: 10.1126/science.2158146.
The role of sodium-calcium exchange at the sarcolemma in the release of calcium from cardiac sarcoplasmic reticulum was investigated in voltage-clamped, isolated cardiac myocytes. In the absence of calcium entry through voltage-dependent calcium channels, membrane depolarization elicited release of calcium from ryanodine-sensitive internal stores. This process was dependent on sodium entry through tetrodotoxin-sensitive sodium channels. Calcium release under these conditions was also dependent on extracellular calcium concentration, suggesting a calcium-induced trigger release mechanism that involves calcium entry into the cell by sodium-calcium exchange. This sodium current-induced calcium release mechanism may explain, in part, the positive inotropic effects of cardiac glycosides and the negative inotropic effects of a variety of antiarrhythmic drugs that interact with cardiac sodium channels. In response to a transient rise of intracellular sodium, sodium-calcium exchange may promote calcium entry into cardiac cells and trigger sarcoplasmic calcium release during physiologic action potentials.
在电压钳制的离体心肌细胞中，研究了肌膜上钠钙交换在心肌肌浆网钙释放中的作用。在没有通过电压依赖性钙通道进入钙的情况下，膜去极化引发了来自对ryanodine敏感的内部储存库的钙释放。这个过程依赖于通过对河豚毒素敏感的钠通道进入的钠。在这些条件下的钙释放也依赖于细胞外钙浓度，提示一种钙诱导触发释放机制，该机制涉及通过钠钙交换使钙进入细胞。这种钠电流诱导的钙释放机制可能部分解释了强心苷的正性肌力作用以及多种与心脏钠通道相互作用的抗心律失常药物的负性肌力作用。响应于细胞内钠的短暂升高，钠钙交换可能促进钙进入心脏细胞并在生理动作电位期间触发肌浆钙释放。
