Verrey F
Institute of Physiology, University of Zürich, Switzerland.
J Membr Biol. 1994 Feb;138(1):65-76. doi: 10.1007/BF00211070.
The effect of antidiuretic hormone on transepithelial Na+ and Cl- transport and its modulation by aldosterone (10(-6) M) was studied in the Xenopus laevis distal nephron cell line A6-C1 by measuring transepithelial electrophysiological parameters and bidirectional anion fluxes. Vasotocin (or vasopressin) induced a biphasic increase in transepithelial short-circuit current (Isc). Early and late effects were potentiated by aldosterone and could be mimicked by forskolin and BrcAMP, implicating cAMP as a mediator. The early increase in Isc (maximum 1-2 min after hormone addition) was resistant to 50 microM amiloride. Electrophysiological experiments with apical ion substitutions or basolateral bumetanide (0.5 mM), as well as flux studies with 125I- or 36Cl-, indicated that this current represented Cl- secretion. The late increase in Isc appeared with a lag of 2-5 min and was maximal after 15-25 min. It corresponded to an increase in Na+ reabsorption, since it was amiloride sensitive. Bidirectional 36Cl- flux measurements in aldosterone-treated monolayers maintained under open-circuit conditions showed that the large vasotocin-induced increase in Cl- permeability led, in these conditions, to a threefold increase of a baseline Cl- reabsorption. This study shows that vasotocin induces in A6-Cl cells both a rapid increase in Cl- permeability and a slower increase in Na+ transport. The Cl- permeability, which leads to Cl- secretion under short-circuit conditions, contributes, under the more physiological open-circuit conditions, to the transport of Na+ by allowing its co-reabsorption with Cl-.
通过测量跨上皮电生理参数和双向阴离子通量，研究了抗利尿激素对非洲爪蟾远端肾单位细胞系A6 - C1上皮细胞跨上皮Na⁺和Cl⁻转运的影响及其受醛固酮（10⁻⁶ M）的调节作用。血管紧张素（或血管加压素）诱导跨上皮短路电流（Isc）出现双相增加。醛固酮可增强早期和晚期效应，且可被福斯高林和BrcAMP模拟，提示cAMP为介导因子。Isc的早期增加（激素添加后1 - 2分钟达到最大值）对50 μM氨氯吡脒有抗性。顶端离子置换或基底侧布美他尼（0.5 mM）的电生理实验，以及¹²⁵I⁻或³⁶Cl⁻的通量研究表明，该电流代表Cl⁻分泌。Isc的晚期增加出现延迟2 - 5分钟，15 - 25分钟后达到最大值。它对应于Na⁺重吸收的增加，因为它对氨氯吡脒敏感。在开路条件下维持的醛固酮处理单层细胞中进行的双向³⁶Cl⁻通量测量表明，血管紧张素诱导的Cl⁻通透性大幅增加，在这些条件下，导致基线Cl⁻重吸收增加三倍。本研究表明，血管紧张素在A6 - Cl细胞中诱导Cl⁻通透性快速增加和Na⁺转运缓慢增加。在短路条件下导致Cl⁻分泌的Cl⁻通透性，在更接近生理的开路条件下，通过允许其与Cl⁻共同重吸收，有助于Na⁺的转运。
