Kupittayanant P, Trafford A W, Díaz M E, Eisner D A
Unit of Cardiac Physiology, University of Manchester, 3.18 Core Technology Facility, 46 Grafton Street, Manchester M13 9NT, UK.
Cell Calcium. 2006 May;39(5):417-23. doi: 10.1016/j.ceca.2006.01.011. Epub 2006 Mar 24.
The aim of this paper was to characterize the pathways that allow Ca(2+) ions to enter the cell at rest. Under control conditions depolarization produced an increase of intracellular Ca concentration (Ca(2+)) that increased with depolarization up to about 0 mV and then declined. During prolonged depolarization the increase of Ca(2+) decayed. This increase of Ca(2+) was inhibited by nifedipine and the calculated rate of entry of Ca increased on depolarization and then declined with a similar time course to the inactivation of the L-type Ca current. We conclude that this component of change of Ca(2+) is due to the L-type Ca current. If intracellular Na was elevated then only part of the change of Ca(2+) was inhibited by nifedipine. The nifedipine-insensitive component increased monotonically with depolarization and showed no relaxation on prolonged depolarization. This component appears to result from Na-Ca exchange (NCX). When the L-type current and NCX were both inhibited (nifedipine and Na-free solution) then depolarization decreased and hyperpolarization increased Ca(2+). These changes of Ca(2+) were unaffected by modifiers of B-type Ca channels such as chlorpromazine and AlF(3) but were abolished by gadolinium ions. We conclude that, in addition to L-type Ca channels and NCX, there is another pathway for entry of Ca(2+) into the ventricular myocyte but this is distinct from the previously reported B-type channel.
本文的目的是描述在静息状态下允许钙离子进入细胞的途径。在对照条件下，去极化使细胞内钙离子浓度（[Ca²⁺]i）升高，该浓度随去极化增加，直至约0 mV，然后下降。在长时间去极化过程中，[Ca²⁺]i的升高逐渐衰减。[Ca²⁺]i的这种升高被硝苯地平抑制，计算得出的钙离子进入速率在去极化时增加，然后随时间进程下降，与L型钙电流的失活情况相似。我们得出结论，[Ca²⁺]i变化的这一成分是由L型钙电流引起的。如果细胞内钠离子浓度升高，那么[Ca²⁺]i变化中只有部分被硝苯地平抑制。硝苯地平不敏感成分随去极化单调增加，在长时间去极化时无衰减。该成分似乎是由钠钙交换（NCX）引起的。当L型电流和NCX均被抑制（硝苯地平和无钠溶液）时，去极化使[Ca²⁺]i降低，超极化使[Ca²⁺]i升高。[Ca²⁺]i的这些变化不受B型钙通道调节剂如氯丙嗪和AlF₃的影响，但被钆离子消除。我们得出结论，除了L型钙通道和NCX外，还有另一条钙离子进入心室肌细胞的途径，但这与先前报道的B型通道不同。
