Greenwood I A, Large W A
Department of Pharmacology and Clinical Pharmacology, St. George's Hospital Medical School, Cranmer Terrace, London SW17 0RE, UK.
Pflugers Arch. 1996 Oct;432(6):970-9. doi: 10.1007/s004240050224.
The time course of calcium-activated chloride "tail" currents (Itail) in single cells of the rabbit portal vein was studied. These currents were activated by the influx of calcium through voltage-dependent calcium channels (VDCCs). At -50 mV, Itail decayed exponentially with a time constant (tau) of 80-100 ms that was independent of amplitude and was similar to the tau of the decay of spontaneous transient inward currents (STICs; calcium-activated chloride currents). The decays of the STIC and Itail had a similar voltage dependence between -50 and -110 mV and were similarly affected by the chloride channel blocker, niflumic acid. However, at more positive potentials (-20 to +40 mV), Itail was sustained for the duration of the test pulse in most cells, in contrast to STICs which decayed exponentially. At very positive potentials (e.g. +100 mV), when little calcium enters the cell through VDCCs, Itail decayed exponentially. Measurement of calcium current (ICa) at various potentials showed that the VDCCs did not inactivate fully at potentials between -20 and +30 mV. We propose that at negative potentials the decay of Itail is determined by slow gating of the chloride channel, but at positive potentials a sustained Itail is produced by persistent influx of calcium through non-inactivating VDCCs.
研究了兔门静脉单个细胞中钙激活氯“尾”电流（Itail）的时间进程。这些电流由钙通过电压依赖性钙通道（VDCCs）内流激活。在-50 mV时，Itail呈指数衰减，时间常数（tau）为80 - 100 ms，该时间常数与电流幅度无关，且与自发瞬时内向电流（STICs；钙激活氯电流）的衰减时间常数相似。在-50至-110 mV之间，STIC和Itail的衰减具有相似的电压依赖性，并且受到氯通道阻滞剂氟尼酸的影响相似。然而，在更正的电位（-20至+40 mV）下，与呈指数衰减的STICs不同，大多数细胞中的Itail在测试脉冲持续期间持续存在。在非常正的电位（例如+100 mV）下，当通过VDCCs进入细胞的钙很少时，Itail呈指数衰减。在不同电位下测量钙电流（ICa）表明，VDCCs在-20至+30 mV之间的电位下并未完全失活。我们提出，在负电位下，Itail的衰减由氯通道的缓慢门控决定，但在正电位下，持续的钙通过非失活的VDCCs内流产生持续的Itail。
