Miyamoto H, Racker E
J Membr Biol. 1982;66(3):193-201. doi: 10.1007/BF01868494.
Ca2+ -induced Ca2+ release at the terminal cisternae of skeletal sarcoplasmic reticulum was demonstrated using heavy sarcoplasmic reticulum vesicles. Ca2+ release was observed at 10 mum Ca2+ in the presence of 1.25 mm free Mg2+ and was sensitive to low concentrations of ruthenium red and was partially inhibited by valinomycin. These results suggest that the Ca2+ -induced Ca2+ release is electrogenic and that an inside negative membrane potential created by the Ca2+ flux opens a second channel that releases Ca2+. Results in support of this formulation were obtained by applying a Cl- gradient or K+ gradient to sarcoplasmic reticulum vesicles to initiate Ca2+ release. Based on experiments the following hypothesis for the excitation-contraction coupling of skeletal muscle was formulated. On excitation, small amounts of Ca2+ enter from the transverse tubule and interact with a Ca2+ enter from the transverse tubule and interact with a Ca2+ receptor at the terminal cisternae and cause Ca2+ release (Ca2+ -induced Ca2+ release). This Ca2+ flux generates an inside negative membrane potential which opens voltage-gated Ca2+ channels (membrane potential-dependent Ca2+ release) in amounts sufficient for contraction.
利用重肌浆网囊泡证明了骨骼肌肌浆网终末池的钙诱导钙释放。在1.25 mM游离镁存在的情况下，在10 μM钙时观察到钙释放，且对低浓度钌红敏感，并部分受缬氨霉素抑制。这些结果表明，钙诱导钙释放是电生性的，由钙通量产生的膜内负电位打开了第二个释放钙的通道。通过对肌浆网囊泡施加氯离子梯度或钾离子梯度以引发钙释放，获得了支持该假说的结果。基于实验，提出了如下骨骼肌兴奋-收缩偶联假说。兴奋时，少量钙从横管进入，与终末池处的钙受体相互作用并引起钙释放（钙诱导钙释放）。这种钙通量产生膜内负电位，该电位打开电压门控钙通道（膜电位依赖性钙释放），释放量足以引起收缩。
