Ca2+ influx during the cardiac action potential in guinea pig ventricular myocytes
Ca2+ influx during the cardiac action potential in guinea pig ventricular myocytes
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DOI：
10.1161/01.res.79.2.194
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发表时间：
1996-08-01
影响因子：
20.1
通讯作者：
Cannell, MB
中科院分区：
文献类型：
--
作者：
Grantham, CJ;Cannell, MB
L型钙电流（I-Ca）和Na+/Ca ~（2+）交换对心肌动作电位（AP）过程中Ca ~（2+）内流的相对贡献尚不清楚。在这项研究中，我们使用了一个AP记录在生理条件下的命令电压施加到电压钳位心室肌细胞。I-Ca（硝苯地平敏感性膜电流）在AP期间具有复杂的多相时程。峰值I-Ca通常为4 pA/pF，之后在细胞范围内的Ca 2+瞬变的上升阶段期间迅速下降（至峰值的约60%），然后增加至第二个更持续的组分。I-Ca的初始下降对肌浆网（SR）释放的Ca 2+量敏感，以及降低Ca 2+瞬变幅度的条件（如休息或短暂应用咖啡因）增加通过I-Ca的净Ca 2+内流在AP开始时的Na+/Ca 2+交换电流的解剖表明，通过Na+/Ca 2+交换的Ca 2+内流小于30%。这是因为I-Ca。根据这些数据，我们认为I-Ca是触发SR Ca ~（2+）释放的Ca ~（2+）的主要来源，即使是与AP相关的高度去极化的膜电位。然而，通过Na+/Ca 2+交换的Ca 2+流入是不可忽略的，并且可能激活SR的一些Ca 2+释放，特别是当Ic降低时。我们建议，SR Ca 2+释放抑制I-Ca在同一拍，从而提供了一个负反馈机制，可能有助于限制Ca 2+内流以及调节存储在SR内的Ca 2+的量。
The relative contributions of L-type Ca2+ current (I-Ca) and Na+/Ca2+ exchange to Ca2+ influx during the cardiac action potential (AP) are unknown. In this study, we have used an AP recorded under physiological conditions as the command voltage applied to voltage-clamped ventricular myocytes. I-Ca (measured as nifedipine-sensitive membrane current) had a complex multiphasic time course during the AP. Peak I-Ca was typically 4 pA/pF, after which it rapidly declined (to about 60% of peak) during the rising phase of the cell-wide Ca2+ transient before increasing to a second, more sustained component. The initial decline in I-Ca was sensitive to the amount of Ca2+ released by the sarcoplasmic reticulum (SR), and conditions that reduce the amplitude of the Ca2+ transient (such as rest or brief application of caffeine) increased net Ca2+ influx via I-Ca Dissection of the Na+/Ca2+ exchange current at the start of the AP suggested that Ca2+ influx via Na+/Ca2+ exchange is less than 30% of that due to I-Ca. From these data, we suggest that I-Ca is the primary source of Ca2+ that triggers SR Ca2+ release, even al the highly depolarized membrane potentials associated with the AP. However, Ca2+ influx via Na+/Ca2+ exchange is not negligible and may activate some Ca2+ release from the SR, especially when Ic, is reduced. We propose that SR Ca2+ release inhibits I-Ca within the same beat, thereby providing a negative feedback mechanism that may serve to limit Ca2+ influx as well as to regulate the amount of Ca2+ stored within the SR.