首页> 美国卫生研究院文献>The Journal of Physiology >Change in intracellular calcium ion concentration induced by caffeine and rapid cooling in frog skeletal muscle fibres.
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Change in intracellular calcium ion concentration induced by caffeine and rapid cooling in frog skeletal muscle fibres.

机译:咖啡因引起的细胞内钙离子浓度变化以及青蛙骨骼肌纤维的快速冷却。

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摘要

In a single skeletal muscle fibre treated with concentrations of caffeine below threshold for caffeine contracture, rapid lowering of the temperature of the bathing solution from 18 degrees C to below 5 degrees C induced a contracture (rapid cooling contracture). Intracellular Ca2+ concentration ([Ca2+]i) was recorded during rapid cooling contracture using aequorin. Low concentrations of caffeine often caused a slight elevation of the light signal in resting muscle without detectable tension. During rapid cooling contracture, the change in light signal occurred in three phases. The first phase was a transient change of [Ca2+]i accompanying slight tension. During the second phase, the light signal slowly increased as cooling produced maximum tension development. The third phase was an additional light signal induced after the second phase, even though the tension was saturated. The second and third phases were more sensitive to low concentrations of procaine (0.2-0.5 mM) than the first phase. Synchronous oscillations of light and tension were often observed during the second phase. The light signal during rapid cooling contracture was only slightly affected by long incubation in Ca-free or Ca-rich solutions. These results are interpreted as follows. A low concentration of caffeine elevates cytoplasmic resting Ca2+ level without tension development. The oscillations of light and tension often observed in the second phase might represent a cyclic release of Ca2+ from the sarcoplasmic reticulum (s.r.). The third phase is considered to be due to a massive Ca2+ release by a Ca-induced Ca-release mechanism which might be similar to that in skinned fibres. The second phase is probably essential for generation of rapid cooling contracture tension and the third phase represents an excess Ca2+ for tension development.
机译:在用咖啡因浓度低于咖啡因挛缩阈值处理的单根骨骼肌纤维中,沐浴液的温度从18摄氏度快速降低到5摄氏度以下会引起挛缩(快速冷却挛缩)。使用水母发光蛋白在快速冷却挛缩期间记录细胞内Ca2 +浓度([Ca2 +] i)。低浓度的咖啡因通常会导致静息肌的光信号轻微升高,而无法检测到张力。在快速挛缩期间,光信号的变化发生在三个阶段。第一阶段是[Ca2 +] i的瞬时变化并伴有轻微的张力。在第二阶段,随着冷却产生最大的张力,光信号逐渐增加。第三阶段是第二阶段之后产生的附加光信号,即使张力已饱和。与第一阶段相比,第二和第三阶段对低浓度的普鲁卡因(0.2-0.5 mM)更加敏感。在第二阶段经常观察到光和张力的同步振荡。在无钙或富含钙的溶液中长时间孵育后,快速冷却挛缩期间的光信号仅受到轻微影响。这些结果解释如下。低浓度的咖啡因可提高细胞质的静息Ca2 +水平,而不会产生紧张。在第二阶段中经常观察到的光和张力的振荡可能表示Ca2 +从肌浆网(s.r.)循环释放。第三阶段被认为是由于Ca诱导的Ca释放机制大量释放了Ca2 +,这可能与表皮纤维相似。第二阶段对于快速冷却挛缩张力的产生可能是必不可少的,而第三阶段则表示产生张力时过量的Ca2 +。

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