Termination of Ca2+ release during Ca2+ sparks in rat ventricular myocytes
Termination of Ca2+ release during Ca2+ sparks in rat ventricular myocytes
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DOI：
10.1111/j.1469-7793.1998.667bs.x
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发表时间：
1998-03-15
影响因子：
5.5
通讯作者：
Györke, S
中科院分区：
文献类型：
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作者：
Lukyanenko, V;Wiesner, TF;Györke, S
1. 共聚焦Ca2+成像用于测量自发释放事件（Ca2+火花）在fluo-3负载的离体大鼠心室肌细胞2。Ca2+火花下的微观Ca2+释放通量是通过采用以前用于描述细胞平均Ca2+瞬态的宏观Ca2+释放的方法得出的。根据SR Ca2+加载条件，局部释放通量的大小从2到5 μ M ms（-1）不等。自发激活后，释放通量迅速衰减（tau = 6-12 ms）。发现释放通量的终止率与通量的大小直接相关（r(2) = 0.88）。在FK506的存在下，局部释放通量的终止速率减慢，FK506是一种已知可以在体外减少SR Ca2+通道失活的化合物。这些结果表明火花释放通量的终止不是由于自发的随机衰变过程或局部Ca2+从SR中耗尽，而是涉及一个主动的熄灭机制，如Ca2+依赖的失活或适应。
1. Confocal Ca2+ imaging was used to measure spontaneous release events (Ca2+ sparks) in fluo-3-loaded isolated rat ventricular myocytes.2. The microscopic Ca2+ release flux underlying Ca2+ sparks was derived by adapting the methods used previously to describe macroscopic Ca2+ release from cell-averaged Ca2+ transients.3. The magnitude of the local release fluxes varied from 2 to 5 mu M ms(-1), depending on SR Ca2+ loading conditions. Following spontaneous activation, the release flux rapidly decayed (tau = 6-12 ms). The rate of termination of release flux was found to be directly related to the magnitude of the flux (r(2) = 0.88).4. The rate of termination of local release flux was slowed in the presence of FK506, a compound that is known to reduce inactivation of SR Ca2+ channels in vitro.5. These results suggest that termination of release flux during sparks is not due to a spontaneous stochastic decay process or local depletion of Ca2+ from the SR, but rather involves an active extinguishing mechanism such as Ca2+-dependent inactivation or adaptation.