Nihonyanagi K, Oba T
Department of Microbiology, Kyoto Prefectural Medical University, Japan.
Eur J Pharmacol. 1996 Sep 12;311(2-3):271-6. doi: 10.1016/0014-2999(96)00435-9.
Effects of Au3+ on Ag(+)-induced contractures and Ca2+ release channel activity in the sarcoplasmic reticulum were studied in frog skeletal muscles. Single fibres spontaneously produced phasic and tonic contractures upon addition of 5-20 microM Ag+ or more than 50 microM Au3+. Simultaneous application of 5 microM Ag+ and 20 microM Au3+ inhibited contractures induced by Ag+. Au3+ applied immediately after development of Ag(+)-induced contractures shortened the duration of the phasic contracture and markedly decreased the subsequent tonic contracture. Pretreatment of fibres with Au3+ inhibited the Ag(+)-induced phasic contracture. Ca2+ release channels incorporated into planar lipid bilayers were activated in response to Au3+ at 20 to 200 microM. A close relationship was observed between Ca2+ release channel open probability and amplitude of the Au(3+)-induced tonic contracture. Channel activity was inhibited by 5 microM ruthenium red. We conclude that extracellular Au3+ at low concentrations modifies the interaction of Ag+ with voltage sensors in the transverse tubules to inhibit the Ag(+)-induced contracture and, if it enters the cell, Au3+ may directly activate the sarcoplasmic reticulum Ca2+ release channel to partially contribute to the tonic contracture.
在青蛙骨骼肌中研究了Au3+对Ag(+)诱导的挛缩以及肌浆网中Ca2+释放通道活性的影响。加入5 - 20微摩尔/升的Ag+或超过50微摩尔/升的Au3+后,单根肌纤维会自发产生相位性和强直性挛缩。同时施加5微摩尔/升的Ag+和20微摩尔/升的Au3+可抑制由Ag+诱导的挛缩。在Ag(+)诱导的挛缩出现后立即施加Au3+,可缩短相位性挛缩的持续时间,并显著降低随后的强直性挛缩。用Au3+对肌纤维进行预处理可抑制Ag(+)诱导的相位性挛缩。整合到平面脂质双分子层中的Ca2+释放通道在20至200微摩尔/升的Au3+作用下被激活。观察到Ca2+释放通道开放概率与Au(3+)诱导的强直性挛缩幅度之间存在密切关系。通道活性被5微摩尔/升的钌红抑制。我们得出结论,低浓度的细胞外Au3+会改变Ag+与横管中电压传感器的相互作用,从而抑制Ag(+)诱导的挛缩,并且如果Au3+进入细胞,它可能直接激活肌浆网Ca2+释放通道,对强直性挛缩有部分作用。