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细胞外钙和钙通道阻滞剂对青蛙骨骼肌纤维银诱导挛缩的影响。

Effects of extracellular calcium and calcium channel blocker on silver-induced contractures in frog skeletal muscle fibers.

作者信息

Oba T, Hotta K

出版信息

Jpn J Physiol. 1987;37(1):125-35. doi: 10.2170/jjphysiol.37.125.

Abstract

The mechanism by which Ag+ induces muscle contracture was elucidated by investigating the effect of external Ca2+ concentration and Ca2+ channel blocker on the maximum tension amplitude in single fibers from frog toe skeletal muscle. Five microM Ag+ induced two different types of contracture in the presence of external Ca2+ more than 0.1 mM, i.e., a phasic and a subsequent tonic contracture. The phasic contracture appeared only in fibers with intact T-tubules immersed in a solution with or without Ca2+ after a lag time of 5.7 +/- 0.9 s (N = 5). The maximum amplitude was 58% of the tetanus tension observed in the same fiber immediately before Ag+ exposure. Diltiazem at high-concentration (100 microM) inhibited the Ag+-induced phasic contracture only to a small extent (17%). The contracture was not affected by 1 microM TTX or 1 mM DAP at all. These results indicate that Na+, K+, and Ca2+ channels on the T-tubular membrane would not be attributed to the phasic tension development induced by Ag+. On the contrary, a tonic contracture did not require intact T-tubules. The amplitude and the rate of rise of the contracture depended on external Ca2+ concentrations and were inhibited by a high concentration of diltiazem. Neither 1 microM TTX nor 1 mM DAP affected them. Therefore, the tonic contracture seems to be triggered by Ca2+ which entered the muscle fiber through the surface but not T-tubular membranes.

摘要

通过研究细胞外Ca2+浓度和Ca2+通道阻滞剂对青蛙趾骨骼肌单纤维最大张力幅度的影响,阐明了Ag+诱导肌肉挛缩的机制。在细胞外Ca2+浓度高于0.1 mM时,5 microM Ag+可诱导出两种不同类型的挛缩,即相性挛缩和随后的强直性挛缩。相性挛缩仅出现在T小管完整的纤维中,在5.7±0.9 s(N = 5)的延迟时间后,纤维浸入含或不含Ca2+的溶液中。最大幅度为Ag+暴露前同一纤维中观察到的强直张力的58%。高浓度(100 microM)的地尔硫䓬仅在很小程度上(17%)抑制Ag+诱导的相性挛缩。该挛缩完全不受1 microM TTX或1 mM DAP的影响。这些结果表明,T小管膜上的Na+、K+和Ca2+通道与Ag+诱导的相性张力发展无关。相反,强直性挛缩不需要完整的T小管。挛缩的幅度和上升速率取决于细胞外Ca2+浓度,并受到高浓度地尔硫䓬的抑制。1 microM TTX和1 mM DAP均不影响它们。因此,强直性挛缩似乎是由通过肌纤维表面而非T小管膜进入的Ca2+触发的。

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