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粘膜溶液中氯离子或钾离子浓度变化对美西螈胆囊上皮细胞水容量的影响。

Effects of changes in mucosal solution Cl- or K+ concentration on cell water volume of Necturus gallbladder epithelium.

作者信息

Cotton C U, Reuss L

机构信息

Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.

出版信息

J Gen Physiol. 1991 Apr;97(4):667-86. doi: 10.1085/jgp.97.4.667.

Abstract

An electrophysiologic technique was used to measure changes in cell water volume in response to isosmotic luminal solution ion replacement. Intracellular Cl- activity (aCl-i) was measured and net flux determined from the changes in volume and activity. Reduction of luminal solution [Cl-] from 98 to 10 mM (Cl- replaced with cyclamate) resulted in a large fall in aCl-i with no significant change in cell water volume. Elevation of luminal solution [K+] from 2.5 to 83.5 mM (K+ replaced Na+) caused a small increase in aCl-i with no change in cell water volume. Exposure of the Necturus gallbladder epithelium to agents that increase intracellular cAMP levels (forskolin and/or theophylline) induces an apical membrane electrodiffusive Cl- permeability accompanied by a fall in aCl-i and cell shrinkage. In stimulated tissues, reduction of luminal solution [Cl-] resulted in a large fall in aCl-i and rapid cell shrinkage, whereas elevation of luminal solution [K+] caused a large, rapid cell swelling with no significant change in aCl-i. The changes in cell water volume of stimulated tissues elicited by lowering luminal solution [Cl-] or by elevating luminal solution [K+] were reduced by 60 and 70%, respectively, by addition of tetraethylammonium (TEA+) to the luminal bathing solution. From these results, we conclude that: (a) In control tissues, the fall in aCl-i upon reducing luminal solution [Cl-], without concomitant cell shrinkage, indicates that the Cl- entry mechanism is electroneutral (Cl-/HCO3-) exchange. (b) Also in control tissues, the small increase in aCl-i upon elevating luminal solution [K+] is consistent with the recent demonstration of a basolateral Cl- conductance. (c) The cell shrinkage elicited by elevation of intracellular cAMP levels results from conductive loss of Cl- (and probably K+). (d) Elevation of cAMP inhibits apical membrane Cl-/HCO-3-exchange activity by 70%. (e) The cell shrinkage in response to the reduction of mucosal solution [Cl-] in stimulated tissues results from net K+ and Cl- efflux via parallel electrodiffusive pathways. (f) A major fraction of the K+ flux is via a TEA(+)-sensitive apical membrane K+ channel.

摘要

采用一种电生理技术来测量细胞水体积对等渗管腔溶液离子置换的变化。测量细胞内氯离子活性(aCl-i),并根据体积和活性的变化确定净通量。将管腔溶液[Cl-]从98 mM降至10 mM(用甜蜜素替代Cl-)导致aCl-i大幅下降,而细胞水体积无显著变化。将管腔溶液[K+]从2.5 mM升高至83.5 mM(K+替代Na+)导致aCl-i略有增加,细胞水体积无变化。将美西螈胆囊上皮暴露于增加细胞内cAMP水平的试剂(福斯高林和/或茶碱)会诱导顶端膜电扩散性Cl-通透性增加,同时aCl-i下降和细胞收缩。在受刺激的组织中,降低管腔溶液[Cl-]会导致aCl-i大幅下降和细胞快速收缩,而升高管腔溶液[K+]会导致细胞迅速大幅肿胀,aCl-i无显著变化。通过向管腔浴液中添加四乙铵(TEA+),受刺激组织因降低管腔溶液[Cl-]或升高管腔溶液[K+]引起的细胞水体积变化分别减少了60%和70%。从这些结果中,我们得出以下结论:(a)在对照组织中,降低管腔溶液[Cl-]时aCl-i下降而无伴随细胞收缩,表明Cl-进入机制是电中性的(Cl-/HCO3-)交换。(b)同样在对照组织中,升高管腔溶液[K+]时aCl-i略有增加与最近证明的基底外侧Cl-电导一致。(c)细胞内cAMP水平升高引起的细胞收缩是由于Cl-(可能还有K+)的传导性丢失。(d)cAMP升高会使顶端膜Cl-/HCO3-交换活性抑制70%。(e)受刺激组织中因黏膜溶液[Cl-]降低引起的细胞收缩是由于K+和Cl-通过平行电扩散途径的净流出。(f)大部分K+通量是通过对TEA+敏感的顶端膜K+通道。

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