Studies of sodium channels in rabbit urinary bladder by noise analysis.
Studies of sodium channels in rabbit urinary bladder by noise analysis.
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通过噪声分析研究兔膀胱钠通道。
DOI：
10.1007/bf01868770
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Diamond,JM
中科院分区：
文献类型：
--
作者：
Lewis,SA;Ifshin,MS;Loo,DD;Diamond,JM
本文用噪声分析法研究了家兔膀胱钠通道。短路电流（Isc）有两个组成部分，相应地，顶端Na+进入也有两个组成部分，一个是阿米洛利敏感的（分别称为IA和A通道），另一个是阿米洛利不敏感的（分别称为IL和泄漏途径）。泄漏路径产生tol/f噪声，而阿米洛利存在下的A通道产生洛伦兹噪声。A通道的两态模型很好地解释了洛伦兹噪声的拐角频率和平台值如何随阿米洛利浓度而变化。单沟道电流为0.64 pA，并且导电沟道密度为每个单元40个拷贝的数量级。氨苯蝶啶单独阻断A通道，增加外部Na+会降低A通道的数量，但不会降低A通道的单通道渗透性。流体静压脉冲（“冲压”）增加了两条路径的数量。本文比较了不同类型上皮细胞A通道的噪声分析结果，并讨论了l/f噪声的作用机制。提示A通道在细胞内合成，储存于胞内囊泡中，在微丝作用下随囊泡膜或从囊泡膜转移到顶膜，并降解进入渗漏通道，被尿液冲洗或破坏。A通道从PNa/PK = 30开始，在PNa/PK达到自由溶液迁移率比（= 0.7）之前，A通道逐渐失去选择性。这种周转周期作为Na+通道的修复和调节机制发挥作用，类似于大多数细胞内蛋白质通过周转的修复和调节。膜通道的囊泡递送可能在其他几种上皮细胞中起作用。
Sodium channels in rabbit urinary bladder were studied by noise analysis. There are two components of short-circuit current (Isc) and correspondingly two components of apical Na+entry, one amiloride-sensitive (termedIAand the A channel, respectively) and one amiloride-insensitive (ILand the leak pathway, respectively). The leak pathway gives rise tol/fnoise, while the A channel in the presence of amiloride gives rise to Lorentzian noise. A two-state model of the A channel accounts well for how the corner frequency and plateau value of Lorentzian noise vary with amiloride concentration. The single-channel current is 0.64 pA, and the conducting channel density is on the order of 40 copies per cell. Triamterene blocks the A channel alone, and increasing external Na+decreases the number but not the single-channel permeability of the A channel. Hydrostatic pressure pulses (“punching”) increase the number of both pathways. Repeated washing of the mucosal surface removes most of the leak pathway without affecting the A channel.Properties of the A channel revealed by noise analysis of various tight epithelia are compared, and the mechanism ofl/fnoise is discussed. It is suggested that the A channel is synthesized intracellularly, stored in intracellular vesicles, transferred with or from vesicular membrane into apical membrane under the action of microfilaments, and degraded into the leak pathway, which is washed out into urine or destroyed. The A channel starts withPNa/PK∼30 and loses selectivity in stages untilPNa/PKreaches the free-solution mobility ratio (∼0.7) for the leak pathway. This turnover cycle functions as a mechanism of repair and regulation for Na+channels, analogous to the repair and regulation of most intracellular proteins by turnover. Vesicular delivery of membrane channels may be operating in several other epithelia.