Vorobets Z D, Puzyrev S Iu, Kurskiĭ M D
Biokhimiia. 1986 Aug;51(8):1295-301.
The effect of membrane potential on passive Ca2+ transport in isolated cardiac sarcolemmal vesicles was investigated. The membrane potentials were induced by creating potassium gradients across the vesicular membranes in the presence of valinomycin. The fluorescence changes in the voltage-sensitive dye, dis-C3(5), were consistent with the induction of potassium equilibrium potentials. The rate of 45Ca2+ efflux from inside-out vesicles was considerably greater at 0 than at -80 or +55 mV; prepolarization of the membrane to +90 mV did not enhance the 45Ca2+ efflux upon subsequent depolarization. The voltage-dependent 45Ca2+ efflux increased with a rise in internal Ca2+ concentration and exhibited a saturation effect. Furthermore, evaluation of the rate of 45Ca2+ efflux over a wide range of membrane potentials produced a profile similar to that of current-voltage relationships for single calcium channels in isolated cardiomyocytes. It is concluded that the voltage-dependent Ca2+ efflux from the vesicles occurs via Ca2+-channels.
研究了膜电位对分离的心肌肌膜囊泡中被动Ca2+转运的影响。通过在缬氨霉素存在下跨囊泡膜建立钾梯度来诱导膜电位。电压敏感染料dis-C3(5)的荧光变化与钾平衡电位的诱导一致。从内向外囊泡的45Ca2+流出速率在0 mV时比在-80或+55 mV时显著更高；膜预极化到+90 mV在随后去极化时并未增强45Ca2+流出。电压依赖性45Ca2+流出随内部Ca2+浓度升高而增加并表现出饱和效应。此外，在很宽的膜电位范围内评估45Ca2+流出速率产生的曲线类似于分离心肌细胞中单个钙通道的电流-电压关系曲线。得出的结论是，囊泡中电压依赖性Ca2+流出通过Ca2+通道发生。
