Isenberg G
Pflugers Arch. 1977 Oct 19;371(1-2):77-85. doi: 10.1007/BF00580775.
The pacemaker tail current of sheep Purkinje fibres became larger when CaCl2 was injected intracellularly by pressure, whereas it was reduced or even abolished by injection of K-EGTA. The analysis of the [Ca2+]k-induced changes in the steady state activation (s infinity) curve suggested that the effect could not be explained on the basis of internal screening of surface charges. The position of the s infinity-curve on the potential axis remained almost unchanged after the injection of CaCl2 or K-EGTA. On the other hand, the vertical amplitude of the s infinity-curve on the current axis, proportional to gK2, was enlarged during CaCl2 injections and strongly diminished by K-EGTA injections. Ca injection displaced the fully deactivated part of the s infinity-curve to larger outward current which corresponds to an increase in gK1. EGTA injection reduced gI1. The results correspond to a [Ca2+]i-sensitive potassium permeability. A possible interpretation is that [Ca2+]i controls Ca-binding near the inner mouth of a potassium channel and that the binding is followed by a change in the channel's configuration from a closed to an open state.
当通过压力向绵羊浦肯野纤维细胞内注射氯化钙时,其起搏器尾电流增大,而注射K-EGTA时,尾电流减小甚至消失。对[Ca2+]k诱导的稳态激活(s无穷大)曲线变化的分析表明,这种效应不能基于表面电荷的内部屏蔽来解释。注射氯化钙或K-EGTA后,s无穷大曲线在电位轴上的位置几乎保持不变。另一方面,s无穷大曲线在电流轴上的垂直幅度与gK2成正比,在注射氯化钙时增大,而在注射K-EGTA时大幅减小。注射钙使s无穷大曲线完全失活的部分移向更大的外向电流,这对应于gK1的增加。注射EGTA降低了gI1。这些结果与[Ca2+]i敏感的钾通透性一致。一种可能的解释是,[Ca2+]i控制钾通道内口附近的钙结合,并且这种结合之后通道构型从关闭状态变为开放状态。