Apical membrane potassium and chloride permeabilities in surface cells of rabbit descending colon epithelium.
Apical membrane potassium and chloride permeabilities in surface cells of rabbit descending colon epithelium.
复制标题
兔降结肠上皮表面细胞顶膜钾和氯渗透性。
DOI：
10.1113/jphysiol.1985.sp015560
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Wills,NK
中科院分区：
文献类型：
--
作者：
Wills,NK
兔降结肠表面细胞的顶膜具有与阿米洛利可阻断Na+通道平行的显著离子电导。负责阿米洛利不敏感电导的离子的身份未知。本文的目的是使用常规和离子敏感微电极技术评估K+和Cl-穿过该膜的渗透性和净驱动力。细胞内Cl-活性（aiCl）平均为23 +/-2 mM，平衡电位（ECl）为-38 +/-2 mV。这一数值小于先前对电动势（e.m.f.）的估计。阿米洛利不敏感通路（英语：Amiloride insensitive pathway）-50 mV）。因此，单独的Cl-无法解释阿米洛利不敏感的电导。用葡萄糖酸盐替代servastine溶液中的Cl-，使aiCl降至17 +/-2.8 mM。通过在粘膜浴中替代或在两种溶液中替代，aiCl降至约1 mM。结果表明基底外侧膜中的Cl-电导较低，与该上皮的先前电生理学研究一致。与Cl-相反，K+的化学驱动力足够大，足以支持电动势。阿米洛利不敏感途径（K+平衡电位，EK =-66 mV）。基底外侧膜电位（Vbl）、EK和细胞内K+活性（aiK）在基底外侧Na-K泵抑制后平行降低，证明Vbl主要是由于K+扩散电位。在存在Serpine 10（-4）M-哇巴因的情况下，aiK似乎保持在平衡以上，并且在向Serpine浴中加入Ba 2+后增加一倍以上。用KCl或葡萄糖酸盐林格氏溶液替换粘膜浴溶液，大大恢复了先前用哇巴因治疗过的组织中的Vbl和跨上皮电位（VT）。在粘膜浴中加入四乙铵可降低VT的恢复，增加跨上皮阻力（RT）。上述结果提示，离子穿过兔结肠表面上皮细胞顶膜至少有四条途径。这些是：（1）阿米洛利敏感性Na+通道，（2）K+电导，（3）Cl-从管腔到细胞内部的电中性摄取和（4）K+主动转运机制，也是从管腔到细胞内部。
The apical membranes of surface cells in the rabbit descending colon possess a significant ionic conductance in parallel to amiloride‐blockable Na+ channels. The identity of the ion(s) responsible for the amiloride‐insensitive conductance is unknown. The purpose of the present paper was to assess the permeability and net driving forces for K+ and Cl‐ across this membrane using conventional and ion‐sensitive micro‐electrode techniques. Intracellular Cl‐ activity (aiCl) averaged 23 +/‐ 2 mM with an equilibrium potential (ECl) of ‐38 +/‐ 2 mV. This value is less than previous estimates of the electromotive force (e.m.f.) of the amiloride‐insensitive pathway (ca. ‐50 mV). Consequently, Cl‐ alone cannot account for the amiloride‐insensitive conductance. Replacement of Cl‐ by gluconate in the serosal solution decreased aiCl to 17 +/‐ 2.8 mM. aiCl was lowered to approximately 1 mM by replacement in the mucosal bath or by replacement in both solutions. The results indicate a low Cl‐ conductance in the basolateral membrane, in agreement with previous electrophysiological studies of this epithelium. In contrast to Cl‐, the chemical driving force for K+ was large enough to support the e.m.f. of the amiloride‐insensitive pathway (K+ equilibrium potential, EK = ‐66 mV). The basolateral membrane potential (Vbl), EK and the intracellular K+ activity (aiK) were decreased in parallel following inhibition of the basolateral Na‐K pump, providing evidence that Vbl is largely due to a K+ diffusion potential. In the presence of serosal 10(‐4) M‐ouabain, aiK appeared to remain above equilibrium and more than doubled after addition of Ba2+ to the serosal bath. Replacement of the mucosal bathing solution with KCl or gluconate Ringer solution largely restored Vbl and the transepithelial potential (VT) in tissues which had been previously treated with ouabain. The restoration of VT was decreased and the transepithelial resistance (RT) was increased by addition of tetraethylammonium to the mucosal bath. The above results suggest that there are at least four routes for ion movement across the apical membrane of rabbit colon surface epithelial cells. These are: (1) an amiloride‐sensitive Na+ channel, (2) a K+ conductance, (3) electroneutral uptake of Cl‐ from lumen to cell interior and (4) an active K+ transport mechanism, also from lumen to cell interior.