Control of intracellular ionized calcium concentration by sarcolemmal and intracellular mechanisms.
Control of intracellular ionized calcium concentration by sarcolemmal and intracellular mechanisms.
复制标题
通过肌膜和细胞内机制控制细胞内离子钙浓度。
DOI：
10.1016/s0022-2828(84)80702-6
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发表时间：
1984
影响因子：
5
通讯作者：
Allen,DG
中科院分区：
文献类型：
--
作者：
Eisner,DA;Orchard,CH;Allen,DG
用发光蛋白水母发光蛋白测定雪貂乳头肌静息状态细胞内游离钙浓度（[Ca ~（2+）]i），研究了[Ca ~（2+）]i的调节。升高[Ca ~（2+）]_0使[Ca ~（2+）]_i和张力先迅速增加，然后逐渐下降到稳定水平。这种[Ca 2 +] i的二次下降归因于已知的[Na+]i下降所产生的Na−Ca交换中Ca进入的二次减少。用K替代外部Na，产生了[Ca ~（2+）] i和张力的大的瞬时增加，然后自发地衰减到接近静息水平。如果在用氰化物和脱氧葡萄糖抑制代谢后除去Na，那么张力和[Ca 2 +]都不能恢复。线粒体解偶联剂FCCP加入到无钠溶液中的肌肉中产生张力的逐渐上升，但延迟许多分钟后才升高[Ca 2 +] i。同样，咖啡因也不升高[Ca 2 +]i。这些实验不支持静息[Ca 2 +] i在无Na溶液中的调节仅取决于[Ca 2 +]i的细胞内螯合的假设。在暴露于无钠溶液后，在含钠溶液中引起的第一次抽搐远大于对照，并且与归因于在无钠溶液中肌浆网的钙负荷增加的大钙瞬变相关。在无钠溶液中[Ca ~（2+）] i的升高伴随着[Ca ~（2+）] i和张力的自发波动，频率约为3 Hz。这些波动被干扰肌浆网功能的药物如咖啡因或ryanodine消除。这些结果提供了直接的证据，自发释放钙从肌浆网推断从以前的，不太直接，工作。
The regulation of the resting intracellular ionized calcium concentration ([Ca2+]i) has been studied in ferret papillary muscle using the photoprotein aequorin to measure [Ca2+]i. Elevating [Ca2+]0produced an initial rapid increase of [Ca2+]iand tension which then decayed to a steady level. This secondary fall of [Ca2+]iis attributed to a secondary decrease of Ca entry on Na−Ca exchange produced by the known fall of [Na+]i. Replacing external Na by K produced a large transient increase of both [Ca2+]iand tension which then decayed spontaneously to near the resting level. If Na was removed after metabolic inhibition with cyanide and deoxyglucose then neither tension nor [Ca2+]irecovered. The addition of the mitochondrial uncoupler FCCP to a muscle in Na-free solution produced a gradual rise of tension but only elevated [Ca2+]iafter a delay of many minutes. Similarly caffeine did not elevate [Ca2+]i. These experiments do not support the hypothesis that the regulation of resting [Ca2+]iin Na-free solutions depends solely on intracellular sequestration of [Ca2+]i. The first twitch elicited in Na-containing solutions after exposure to Na-free solution was much larger than control and was associated with a large Ca transient attributed to increased loading of the sarcoplasmic reticulum with Ca in the Na-free solution. The elevation of [Ca2+]iin Na-free solutions was accompanied by spontaneous fluctuations of both [Ca2+]iand tension with a frequency of about 3 Hz. These fluctuations were abolished by drugs such as caffeine or ryanodine which interfere with sarcoplasmic reticulum function. These results provide direct evidence for the spontaneous release of Ca from the sarcoplasmic reticulum inferred from previous, less direct, work.