SLOW INWARD CALCIUM CURRENTS HAVE NO OBVIOUS ROLE IN MUSCLE EXCITATION CONTRACTION COUPLING
SLOW INWARD CALCIUM CURRENTS HAVE NO OBVIOUS ROLE IN MUSCLE EXCITATION CONTRACTION COUPLING
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DOI：
10.1038/298292a0
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发表时间：
1982-01-01
期刊：
影响因子：
64.8
通讯作者：
GARCIA, MD
中科院分区：
文献类型：
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作者：
GONZALEZSERRATOS, H;VALLEAGUILERA, R;GARCIA, MD
有人提出，在动作电位过程中，钙离子流入肌纤维可能会引发收缩。然而，当EGTA将外部Ca 2+降低到10− 8 M时，纤维可以产生正常的抽搐数分钟。然而，已经证明了收缩过程中明显的Ca 2+内流4，5，并且已经发现相位骨骼肌具有向内的钙电流（伊卡）6，7，其可以引起钙尖峰8。在某些条件下，用80-90 mM EGTA减少外部Ca 2+导致兴奋-收缩（e-c）偶联的可逆阻断9，导致一些作者推测7，9- 11细胞外Ca 2+由于ICamay而移动到肌浆中可能参与触发收缩的e-c偶联机制。这一命题进一步支持的本地化的钙在T-系统，它规避了延迟的问题，由于钙扩散的表面膜。我们现在已经研究了ICA是否在启动或维持抽搐肌纤维收缩中具有明确的作用。我们的方法是用钙阻滞剂地尔硫卓（Herbesser）减少或消除ICA，并观察抽搐、强直和钾挛缩张力如何受到影响。我们发现，钙离子阻断剂可以降低或消除I C，但相同浓度的药物会增强抽搐、强直和挛缩。因此，我们的结论是，ICa在电子-电荷耦合中没有作用。关于这些结果的初步报告已在其他地方提出12。
It has been proposed1that an influx of calcium ions into twitch muscle fibres during an action potential might initiate contraction. However, when external Ca2+is lowered to 10−8M with EGTA, the fibres can produce normal twitches for many minutes2,3. Nevertheless, a clear Ca2+influx during contraction has been demonstrated4,5, and it has been found that phasic skeletal muscle has an inward calcium current (ICa)6,7which can give rise to calcium spikes8. In certain conditions, a reduction in external Ca2+with 80–90 mM EGTA results in reversible blockade of excitation–contraction (e–c) coupling9, leading some authors to suggest7,9–11that extracellular Ca2+moved into the myoplasm due toICamay be involved in the e–c coupling mechanism that triggers contraction. This proposition was further supported by the localization ofICain the T-system, which circumvented the problem of the delay due to calcium diffusion from the surface membrane. We have now investigated whetherICahas a clear role in initiating or sustaining contractions in twitch muscle fibres. Our approach was to decrease or eliminateICawith the calcium-blocking agent diltiazem (Herbesser) and to see how the twitch, tetanic and potassium-contracture tensions were affected. We found thatICacould be decreased or cancelled with the calcium-blocking agent, but that the same concentration of the drug potentiated the twitch, tetanus and contractures. We conclude, therefore, thatICahas no role in e–c coupling. A preliminary report of these results has been presented elsewhere12.