Effects of aldosterone on the impedance properties of cultured renal amphibian epithelia.
Effects of aldosterone on the impedance properties of cultured renal amphibian epithelia.
复制标题
醛固酮对培养的肾两栖动物上皮细胞阻抗特性的影响。
DOI：
10.1007/bf00231874
复制
发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Millinoff,LP
中科院分区：
文献类型：
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作者：
Wills,NK;Purcell,RK;Clausen,C;Millinoff,LP
培养的肾两栖细胞株A6已被证明有利于研究Na+转运调节。在本研究中，评估了醛固酮作用对该上皮的上皮电特性的影响。具体而言，确定醛固酮作用的时间过程，并使用经上皮等效电路方法和阻抗分析技术评估慢性（10-18天）醛固酮升高的影响。短期（<4小时）暴露于醛固酮（0.1μm）可使阿米洛利敏感短路电流（Isc）增加两倍以上，并使上皮电导（GT）增加约12%。在慢性醛固酮暴露的上皮中，isandgt的增加得以维持。与先前的报道相反，醛固酮未改变细胞旁耐药（Rj）。这种差异可能与暴露时间较长或本研究中Na+基础转运速率不同有关。与醛固酮缺失（即血清缺失）的对照组相比，醛固酮处理的上皮细胞的顶膜导电性显著增加。顶膜面积（电容）无明显影响。这一发现与醛固酮刺激后膜上传导Na+通道的更高密度（每膜面积的通道数）是一致的。与血清处理的对照组织相比，醛固酮处理组织的基底外侧膜性质没有明显改变。相反，血清剥夺上皮的基底外侧膜特异性电导率（即，基底外侧膜电导率归一化为基底外侧膜电容）明显低于血清处理对照或醛固酮处理组织。慢性醛固酮暴露对A6亚克隆细胞系2F3的影响也进行了评估。与A6上皮类似，在醛固酮刺激后，isc基本翻倍，而erj和细胞驱动力（Ec）不受影响。对照条件下，2F3上皮的顶膜电导率高于A6，但与醛固酮暴露或血清剥夺后的A6无显著差异。这些发现提示2F3和A6上皮对顶膜Na+通道的调节可能存在差异。
The cultured renal amphibian cell line A6 has proven advantageous for studies of Na+transport regulation. In the present study, the effects of aldosterone action on the transepithelial electrical properties of this epithelium were assessed. Specifically, the time course of aldosterone action was determined and the effects of chronic (10–18 day) aldosterone elevation were assessed using transepithelial equivalent circuit methods and impedance analysis techniques.Short-term (<4 hr) exposure to aldosterone (0.1μm) stimulated the amiloride-sensitive short-circuit current (Isc) by over twofold and increased the transepithelial conductance (GT) by approximately 12%. The increases inIscandGTwere maintained in epithelia subjected to chronic aldosterone exposure. In contrast to previous reports, paracellular resistance (Rj) was not altered by aldosterone. This difference may be related to the longer time of exposure or different basal Na+transport rates in the present study.The apical membrane conductance was significantly increased for aldosterone-treated epithelia compared to aldosterone-depleted (i.e., serum-deprived) controls. Apical membrane area (capacitance) was not significantly affected. This finding is consistent with a higher density (number of channels per membrane area) of conducting Na+channels in this membrane following aldosterone stimulation. Basolateral membrane properties were not significantly altered for aldosteronetreated tissues compared to serum-treated control tissues. In contrast, basolateral membrane-specific conductance (i.e., basolateral membrane conductance normalized to basolateral membrane capacitance) was significantly lower for serum-deprived epithelia than for serum-treated controls or aldosterone-treated tissues.The effects of chronic aldosterone exposure were also evaluated for the A6 subclonal cell line, 2F3. Similar to A6 epithelia,Iscwas essentially doubled following aldosterone stimulation whileRjand cellular driving force (Ec) were not affected. Apical membrane conductances under control conditions for 2F3 epithelia were higher than those for A6, but were not significantly different from A6 following aldosterone exposure or serum deprivation. These findings suggest possible differences in the regulation of apical membrane Na+channels for 2F3 and A6 epithelia.