Trón L, Pieri C, Márián T, Balkay L, Emri M, Damjanovich S
Biomedical Cyclotron Laboratory, University Medical School of Debrecen, Hungary.
Mol Immunol. 1990 Dec;27(12):1307-11. doi: 10.1016/0161-5890(90)90035-x.
We have studied a bretylium tosylate induced increase of the membrane potentials of partially depolarized rat, mouse and human lymphocytes, using the potential sensitive dye, bis [1,3, dibutylbarbituric acid-(5) trimethine oxonol]. The extent of this repolarization is dose-dependent and decreased in magnitude as the temp was reduced from 37 degrees C to room temp. The repolarizing effect is inhibited by K(+)-Na(+)-pump blockers or lack of extracellular Na+. Sodium ion channel blockers are effective in abolishing repolarization only if applied prior to, or simultaneously with, bretylium. Activation of Na+/H+ exchange is not involved in the mechanism of the phenomenon as the latter is completely eliminated in the presence of 10 microM amiloride (concn of the diuretics having no measurable inhibition on the action of the exchanger). These data suggest that bretylium opens ligand- and voltage-gated Na+ channels, and repolarization occurs due to higher activity of the K(+)-Na(+)-pump stimulated by the enhanced intracellular Na+ accumulation.
我们使用电位敏感染料双[1,3 - 二丁基巴比妥酸-(5)-三甲川羰花青]，研究了托西溴苄铵诱导部分去极化的大鼠、小鼠和人淋巴细胞膜电位增加的情况。这种复极化的程度呈剂量依赖性，并且当温度从37℃降至室温时，其幅度会减小。复极化效应受到钾钠泵阻滞剂或细胞外钠离子缺乏的抑制。只有在溴苄铵之前或同时应用时，钠离子通道阻滞剂才有效地消除复极化。由于在10微摩尔氨氯地平存在时该现象完全消除（利尿剂浓度对交换体的作用没有可测量的抑制），所以钠氢交换的激活不参与该现象的机制。这些数据表明，溴苄铵打开了配体门控和电压门控的钠离子通道，并且由于细胞内钠离子积累增加刺激钾钠泵活性增强而发生复极化。
