Potassium rectifier currents differ in myocytes of endocardial and epicardial origin.
Potassium rectifier currents differ in myocytes of endocardial and epicardial origin.
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DOI：
10.1161/01.res.70.1.91
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发表时间：
1992
影响因子：
20.1
通讯作者：
Tetsushi Furukawa;Shinichi Kimura;N. Furukawa;A. Bassett;R. J. Myerburg
中科院分区：
文献类型：
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作者：
Tetsushi Furukawa;Shinichi Kimura;N. Furukawa;A. Bassett;R. J. Myerburg
对从猫心内膜和心外膜表面采集的酶促分离的单个心室肌细胞进行全细胞电压钳实验和细胞贴附膜片钳模式下的单通道电流记录。本研究旨在比较心内膜细胞和心外膜细胞的内向整流钾电流（IK 1）和延迟整流钾电流（IK）的特性，并验证IK 1和/或IK的差异特性是导致两种细胞动作电位构型差异的原因。IK 1在内皮细胞中显示出明显的N型电流-电压（I-V）关系，在-80 ~-30 mV之间有明显的外向电流。心外膜细胞的外向电流区域较小，I-V关系呈钝的N型。在单通道电流记录在细胞贴附补丁模式，无论是单一的电流幅度的IK 1，也没有通道开放的概率是不同的心内膜和心外膜细胞之间，这表明在功能通道的数量的差异可能是负责差异IK 1的I-V关系。心内膜细胞和心外膜细胞的IK特性也不同。与心内膜细胞相比，心外膜细胞IK尾电流（IK，tail）（IK的激活）的增长时程明显增强，IK尾电流的失活时程明显延迟。在+20 mV时，IK激活的慢分量的时间常数在内皮细胞中为3，950 +/- 787 msec，在心外膜细胞中为2，746 +/- 689 msec（p <0.05）;在-50 mV时IK失活的相应值分别为1，041 +/-387毫秒和1，959 +/-551毫秒（p小于0.01）。心内膜细胞和心外膜细胞的IK尾稳态激活的电压依赖性相似，表明在任何电位下通道开放的概率在两种细胞类型中没有差异。心外膜细胞完全激活的IK（IK，full）的幅度和密度明显大于心内膜细胞。在复极化至-20 mV时，IK，全振幅在内膜细胞中为452 +/- 113 pA，在心外膜细胞中为578 +/- 135 pA（p <0.05），IK，全密度的相应值分别为2.86 +/- 0.73和4.21 +/- 0.83 microA/cm 2（p <0.05）。非平稳波动分析显示，心内膜和心外膜细胞之间IK单位电流的幅度相似（0.23 +/- 0.07 vs 0.22 +/- 0.03 pA，p = NS）。（400字处截断摘要）
Whole-cell voltage-clamp experiments and single-channel current recordings in cell-attached patch mode were performed on enzymatically dissociated single ventricular myocytes harvested from feline endocardial and epicardial surfaces. The studies were designed to compare the characteristics of inward rectifier K+ current (IK1) and delayed rectifier K+ current (IK) between endocardial and epicardial cells and to test the hypothesis that the differential characteristics of IK1 and/or IK are responsible for the differences in action potential configuration between the two cell types. IK1 in endocardial cells displayed a distinct N-shaped current-voltage (I-V) relation, with a prominent outward current at potentials between -80 and -30 mV. In epicardial cells, an outward current region was much smaller, and the I-V relation demonstrated a blunted N-shaped I-V relation. In single-channel current recordings in cell-attached patch mode, neither unitary current amplitude of IK1 nor probability of channel opening was different between endocardial and epicardial cells, suggesting that the difference in the number of functional channels might be responsible for the differential IK1 I-V relations. The characteristics of IK also differed between endocardial and epicardial cells. The time course of growth of tail current of IK (IK,tail) (activation of IK) was significantly enhanced and that of IK,tail deactivation was delayed in epicardial cells compared with endocardial cells. The time constant of the slow component of IK activation at +20 mV was 3,950 +/- 787 msec in endocardial cells and 2,746 +/- 689 msec in epicardial cells (p less than 0.05); the corresponding values for IK deactivation at -50 mV were 1,041 +/- 387 msec and 1,959 +/- 551 msec, respectively (p less than 0.01). The voltage dependence of steady-state activation of IK,tail was similar between endocardial and epicardial cells, suggesting that the probability of channel opening at any potential was not different in the two cell types. The amplitude and density of fully activated IK (IK,full) were significantly greater in epicardial cells than in endocardial cells. At repolarization to -20 mV, IK,full amplitude was 452 +/- 113 pA in endocardial cells and 578 +/- 135 pA in epicardial cells (p less than 0.05), and the corresponding values for IK,full density were 2.86 +/- 0.73 and 4.21 +/- 0.83 microA/cm2, respectively (p less than 0.05). A nonstationary fluctuation analysis revealed that the amplitude of IK unitary current was similar between endocardial and epicardial cells (0.23 +/- 0.07 versus 0.22 +/- 0.03 pA, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)