Bridge J H, Smolley J R, Spitzer K W
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City 84112.
Science. 1990 Apr 20;248(4953):376-8. doi: 10.1126/science.2158147.
Ventricular myocytes exhibit a nifedipine-sensitive inward calcium current (ICa) and contracture when they are voltage clamped from -40 to 0 millivolt in the presence of caffeine and in the absence of extracellular sodium. However, upon repolarization they fail to relax because neither the sarcoplasmic reticulum nor the sodium-calcium exchange can reduce intracellular calcium. Sudden application of extracellular sodium during the contracture (but after repolarization) causes immediate relaxation and activates a transient inward sodium-calcium exchange current (INa-Ca), whose peak slightly precedes mechanical relaxation. The total charge carried by the nifedipine-sensitive ICa is twice the total charge carried by the transient inward INa-Ca. Assuming an exchange stoichiometry of three sodium to one calcium, these results indicate that all the calcium entering the cell during the initial depolarization is extruded by the sodium-calcium exchange.
在咖啡因存在且细胞外无钠的情况下，当心室肌细胞从 -40 毫伏电压钳制到 0 毫伏时，会表现出硝苯地平敏感的内向钙电流（ICa）和挛缩。然而，复极化后它们无法松弛，因为肌浆网和钠钙交换都不能降低细胞内钙。在挛缩期间（但在复极化之后）突然施加细胞外钠会导致立即松弛，并激活一个短暂的内向钠钙交换电流（INa-Ca），其峰值略先于机械松弛。硝苯地平敏感的 ICa 携带的总电荷量是短暂内向 INa-Ca 携带的总电荷量的两倍。假设交换化学计量为三个钠对一个钙，这些结果表明在初始去极化期间进入细胞的所有钙都通过钠钙交换排出。
