Mouse hepatocyte membrane potential and chloride activity during osmotic stress.

Mouse hepatocyte membrane potential and chloride activity during osmotic stress.
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渗透应激期间小鼠肝细胞膜电位和氯离子活性。

DOI:
10.1152/ajpgi.1992.263.4.g566
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发表时间:
1992
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Wondergem,R
Wondergem,R
中科院分区:
--
文献类型:
--
作者:
Wang,K;Wondergem,R

文献摘要

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渗透压应激时肝细胞跨膜电位(Vm)起渗透压计的作用,部分原因是膜K+电导的变化。这可能有助于驱动跨膜氯离子通量的电动势。为了验证这一点,使用双管离子敏感微电极来测量渗透胁迫作用于小鼠肝脏切片期间细胞内稳态氯活度(AICL)的变化。高渗和低渗条件是通过快速切换到蔗糖浓度分别增加或减少的溶液来创建的。高渗应激[1.4倍对照渗透压(280molmoL/kgH2O)]使肝细胞Vm从-39+/-1降至-21+/-1 mV(SE;n=16)。相应的AICL从19+/-2增加到38+/-3 mm,增加了两倍。这使氯平衡电位(ECL)从-38+/-0.3 mV移动到-19+/-2 mV。低渗应激[0.71x对照渗透压(290molmoL/kgH2O)]使肝细胞Vm%从-28+/-1增加到-46+/-1 mV(SE;n=13只动物)。相应的AICL从17+/-1 mm减少到8+/-1 mm,减少了0.53倍。这使ECL20 mV从-26+/-2变为-46+/-3 mV。因此,肝细胞AICL与Vm处于电化学平衡状态。在加入K(+)通道阻滞剂奎宁或Ba2+后,重复上述配对测量。Ba2+(2 MM)对高渗应激时的Vm和AICL无明显影响,但可显著抑制低渗应激时Vm和AICL的变化。奎宁(0.5 mM)对高渗和低渗应激时Vm和AICL的影响与Ba2+相似。
Hepatocyte transmembrane potential (Vm) during osmotic stress responds as an osmometer, in part because of changes in membrane K+ conductance. This may contribute to the electromotive force that drives transmembrane Cl- fluxes. To test this, double-barreled ion-sensitive microelectrodes were used to measure changes in steady-state intracellular Cl- activity (aiCl) during osmotic stress applied to mouse liver slices. Hyperosmotic and hyposmotic conditions were created by rapidly switching to a solution in which sucrose concentrations were increased or reduced, respectively. Hyperosmotic stress [1.4 x control osmolality (280 mosmol/kgH2O)] decreased hepatocyte Vm 46% from -39 +/- 1 to -21 +/- 1 mV (SE; n = 16 animals). Corresponding aiCl increased twofold from 19 +/- 2 to 38 +/- 3 mM. This shifted the Cl- equilibrium potential (ECl) 19 mV, from -38 +/- 0.3 to -19 +/- 2 mV. Hyposmotic stress [0.71 x control osmolality (290 mosmol/kgH2O)] increased hepatocyte Vm 64% from -28 +/- 1 to -46 +/- 1 mV (SE; n = 13 animals). Corresponding aiCl decreased 0.53-fold from 17 +/- 1 to 8 +/- 1 mM. This shifted the ECl 20 mV from -26 +/- 2 to -46 +/- 3 mV. Thus hepatocyte aiCl is in electrochemical equilibrium with Vm. The paired measurements above were repeated after addition of K(+)-channel blockers quinine or Ba2+. Ba2+ (2 mM) had no effect on either Vm or aiCl during hyperosmotic stress; however, Ba2+ significantly inhibited changes in Vm and aiCl during hyposmotic stress. Effects of quinine (0.5 mM) on Vm and aiCl during both hyperosmotic stress and hyposmotic stress were similar to those of Ba2+.(ABSTRACT TRUNCATED AT 250 WORDS)