Davis C W, Finn A L
J Gen Physiol. 1982 Nov;80(5):733-51. doi: 10.1085/jgp.80.5.733.
In toad urinary bladder epithelium, inhibition of Na transport with amiloride causes a decrease in the apical (Vmc) and basolateral (Vcs) membrane potentials. In addition to increasing apical membrane resistance (Ra), amiloride also causes an increase in basolateral membrane resistance (Rb), with a time course such that Ra/Rb does not change for 1-2 min. At longer times after amiloride (3-4 min), Ra/Rb rises from its control values to its amiloride steady state values through a secondary decrease in Rb. Analysis of an equivalent electrical circuit of the epithelium shows that the depolarization of Vcs is due to a decrease in basolateral electromotive force (Vb). To see of the changes in Vcs and Rb are correlated with a decrease in Na transport, external current (Ie) was used to clamp Vmc to zero, and the effects of amiloride on the portion of Ie that takes the transcellular pathway were determined. In these studies, Vcs also depolarized, which suggests that the decrease in Vb was due to a decrease in the current output of a rheogenic Na pump. Thus, the basolateral membrane does not behave like an ohmic resistor. In contrast, when transport is inhibited during basolateral membrane voltage clamping, the apical membrane voltage changes are those predicted for a simple, passive (i.e., ohmic) element.
在蟾蜍膀胱上皮细胞中，用氨氯吡咪抑制钠转运会导致顶端（Vmc）和基底外侧（Vcs）膜电位降低。除了增加顶端膜电阻（Ra）外，氨氯吡咪还会导致基底外侧膜电阻（Rb）增加，其时间进程使得Ra/Rb在1 - 2分钟内保持不变。在氨氯吡咪作用较长时间后（3 - 4分钟），Ra/Rb通过Rb的二次降低从其对照值升至氨氯吡咪稳态值。对上皮细胞等效电路的分析表明，Vcs的去极化是由于基底外侧电动势（Vb）降低所致。为了观察Vcs和Rb的变化是否与钠转运的降低相关，使用外部电流（Ie）将Vmc钳制为零，并确定氨氯吡咪对通过跨细胞途径的Ie部分的影响。在这些研究中，Vcs也发生了去极化，这表明Vb的降低是由于生电钠泵的电流输出减少所致。因此，基底外侧膜的行为不像欧姆电阻。相反，当在基底外侧膜电压钳制期间转运受到抑制时，顶端膜电压变化是简单的被动（即欧姆）元件所预测的那样。
