Zeiske W, Van Driessche W
Pflugers Arch. 1984 Feb;400(2):130-9. doi: 10.1007/BF00585030.
Na+ transport across abdominal skins of the frog species Rana esculenta and Rana pipiens was analyzed by recording short-circuit current (Isc), transepithelial conductance (Gt), and the current noise generated by the random blockage of apical Na+ channels by the diuretic, amiloride. Specific Na+ current (INa) and conductance (GNa), as reflected by the amiloride-sensitive part of Isc and Gt, respectively, were markedly depressed after addition of some osmotically active substances, like sugars or alcohols to the mucosal Na+-Ringer solution. These hypertonicity-induced reactions were fast and fully reversible, even at mucosal osmolarities of 1 Osmol. With mucosal solutions of moderate hyperosmolarity a recovery of INa and GNa was observed in presence of the osmotic gradient. This "regulatory" current showed to be carried by Na+ through the Na+-specific apical channels. Contrary to the fast current drop during the initial phase of hyperosmotic shocks, the "osmoregulation" was considerably slower. The recovery of INa was only complete at smaller osmotic gradients but became more and more suppressed at higher osmolarities. Steady-state analysis of the kinetics of the Na+-specific current revealed that the current depression by osmotic shocks obeys Michaelis-Menten kinetics. This current depression at high osmolarities, as well as during the initial phase before "osmoregulation" with small osmotic gradients, can be described in terms of a non-competitive inhibition. This was also suggested by Na+-concentration jump experiments indicating a reduction of the maximal, apical Na+ permeability as mechanism of the hypertonicity-induced drop in INa. The INa kinetics after complete "osmoregulation" were, however, indistinguishable from the isotonic control condition.(ABSTRACT TRUNCATED AT 250 WORDS)
通过记录短路电流（Isc）、跨上皮电导（Gt）以及利尿剂氨氯吡脒对顶端Na⁺通道随机阻断所产生的电流噪声，分析了食用蛙和豹蛙腹部皮肤的Na⁺转运情况。分别由Isc和Gt的氨氯吡脒敏感部分所反映的特异性Na⁺电流（INa）和电导（GNa），在向黏膜Na⁺ - 林格溶液中添加一些渗透活性物质（如糖类或醇类）后，明显降低。即使在黏膜渗透压为1 Osmol时，这些高渗诱导的反应也是快速且完全可逆的。在中等高渗的黏膜溶液中，在存在渗透梯度的情况下观察到INa和GNa的恢复。这种“调节性”电流显示是由Na⁺通过Na⁺特异性顶端通道携带的。与高渗休克初始阶段的快速电流下降相反，“渗透调节”要慢得多。INa的恢复仅在较小的渗透梯度下才完全，但在较高渗透压下越来越受到抑制。对Na⁺特异性电流动力学的稳态分析表明，渗透休克引起的电流降低遵循米氏动力学。高渗透压下以及在小渗透梯度“渗透调节”之前的初始阶段的这种电流降低，可以用非竞争性抑制来描述。Na⁺浓度阶跃实验也表明，顶端Na⁺最大通透性降低是高渗诱导INa下降的机制。然而，完全“渗透调节”后的INa动力学与等渗对照条件无明显差异。（摘要截断于250字）
