Yoshioka T, Somlyo A P
Department of Physiology, Tokai University School of Medicine, Kanagawa, Japan.
J Muscle Res Cell Motil. 1987 Aug;8(4):322-8. doi: 10.1007/BF01568888.
A significant decrease in the Ca2+ and increase in the Mg2+ content of the terminal cisternae (TC) of the sarcoplasmic reticulum (SR) during quinine contraction was demonstrated by electron probe analysis of rapidly frozen frog muscles. The extent of Ca2+ release (71% of total) from the TC and the absence of an increase in total cell Ca2+ support the conclusion that quinine contractures are caused by passive efflux of Ca2+ from the SR when the latter is uncompensated due to inhibition of the SR Ca2+ pump by quinine. A rapid warming contraction (RWC) was observed, in the presence of quinine, when the temperature of intact and skinned muscles was increased from about 5 degrees C to 18-23 degrees C. The duration of the latency of quinine contracture, in intact muscle bundles, was approximately 31 s at 3 degrees C and 2 s at 23 degrees C. The results suggest a significant temperature sensitivity of the passive Ca2+ channels of the SR membrane, although an effect of temperature on the lipid partition coefficient of quinine into the SR has not been ruled out.
通过对快速冷冻的青蛙肌肉进行电子探针分析表明，在奎宁收缩过程中，肌浆网（SR）终末池（TC）中的Ca2+含量显著降低，Mg2+含量增加。终末池Ca2+释放的程度（占总量的71%）以及细胞总Ca2+含量未增加，支持了以下结论：当奎宁抑制SR Ca2+泵而使SR无法得到补偿时，奎宁挛缩是由Ca2+从SR被动流出引起的。当完整肌肉和去皮肌肉的温度从约5℃升高到18 - 23℃时，在奎宁存在的情况下观察到快速升温收缩（RWC）。在完整肌束中，奎宁挛缩潜伏期的持续时间在3℃时约为31秒，在23℃时约为2秒。结果表明，SR膜的被动Ca2+通道具有显著的温度敏感性，尽管尚未排除温度对奎宁进入SR的脂质分配系数的影响。
