Modulation of ryanodine-induced Ca2+ release in amphibian skeletal muscle.
Modulation of ryanodine-induced Ca2+ release in amphibian skeletal muscle.
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DOI：
10.1016/0006-291x(87)91467-7
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发表时间：
1987-02
影响因子：
3.1
通讯作者：
K. Hwang;K. Saida;C. van Breemen
中科院分区：
文献类型：
--
作者：
K. Hwang;K. Saida;C. van Breemen
我们研究了兰尼碱对完整和去皮两栖动物骨骼肌张力的影响。100 μM ryanodine（RY）单独在蛙林格氏溶液（FR）中产生的张力在完整肌肉中在1 h：10 min处理时达到峰值，RY增强去极化诱导的张力，并阻止随后的咖啡因诱导的收缩。相反，RY在无钙FR不能产生张力，之后咖啡因产生不可逆的张力。在皮肤纤维中。RY在pCa 6.5产生张力，并取消了随后的咖啡因诱导的收缩：而RY在2 mM EGTA不产生张力。这些数据表明，RY，在Ca 2+的存在下，从SR中释放Ca 2+，导致随后SR中Ca的耗尽。
We examined effects of ryanodine on tension in intact and skinned amphibian skeletal muscle. 100 μM ryanodine (RY) alone in the frog Ringer's solution (FR) produced tension in the intact muscle reaching its peak by 1 h: 10 min treatment with RY augmented depolarization-induced tension and prevented a subsequent caffeine-induced contraction. In contrast, RY in Ca2+-free FR was unable to produce tension, after which caffeine produced irreversible tension. In skinned fibers. RY at pCa 6.5 produced tension and abolished a subsequent caffeine-induced contraction: while RY in 2 mM EGTA did not produce tension. These data indicate that RY, in the presence of Ca2+, releases Ca2+from the SR resulting in subsequent depletion of Ca in the SR.