Metabolic end products inhibit sarcoplasmic reticulum Ca2+ release and [3H]ryanodine binding.
Metabolic end products inhibit sarcoplasmic reticulum Ca2+ release and [3H]ryanodine binding.
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代谢终产物抑制肌浆网 Ca2 释放和 [3H]ryanodine 结合。
DOI：
10.1152/jappl.1995.78.5.1665
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Abramson,JJ
中科院分区：
文献类型：
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作者：
Favero,TG;Zable,AC;Bowman,MB;Thompson,A;Abramson,JJ
肌浆网(SR)钙释放通道功能受运动过程中产生的配体(镁、钙、三磷酸腺苷和氢离子)的调节。我们研究了改变细胞内代谢产物对大白兔骨骼肌肌浆网钙释放、[~3H]兰尼定结合和单钙释放通道活动的影响。增加镁离子浓度(0~4 mM)和降低pH值(7.1~6.5)可抑制肌质网钙离子释放和[~3H]-兰尼定结合。此外，将乳酸浓度从2 mM增加到20 mM，可抑制[~3H]ryanodine与SR囊泡的结合，抑制SR钙释放，并降低单通道开放概率。这些发现表明，破坏兴奋-收缩偶联和减少钙瞬变的细胞内修饰将促进张力发展的下降，并导致肌肉疲劳。此外，我们还发现过氧化氢可诱导钙离子释放并增加[~3H]兰尼定与其受体的结合，提示运动过程中产生的活性氧可能通过改变肌浆网钙离子释放通道的正常门控而损害肌肉功能。
Sarcoplasmic reticulum (SR) Ca2+ release channel function is modified by ligands (Mg2+, Ca2+, ATP, and H+) that are generated during a bout of exercise. We have examined the effects of changing intracellular metabolites on Ca2+ release, [3H]ryanodine binding, and single-Ca2+ release channel activity of SR isolated from white rabbit skeletal muscle. Increasing Mg2+ (from 0 to 4 mM) and decreasing pH (7.1–6.5) inhibited SR Ca2+ release and [3H]-ryanodine binding. In addition, increasing lactate concentrations from 2 to 20 mM inhibited [3H]ryanodine binding to SR vesicles, inhibited SR Ca2+ release, and decreased the single-channel open probability. These findings suggest that intracellular modifications that disrupt excitation-contraction coupling and decrease Ca2+ transients will promote a decline in tension development and contribute to muscle fatigue. In addition, we show that hydrogen peroxide induces Ca2+ release and increases [3H]ryanodine binding to its receptor, suggesting that reactive oxygen species produced during exercise may compromise muscle function by altering the normal gating of the SR Ca2+ release channel.