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XB-ART-21618
J Membr Biol 1994 Feb 01;1381:65-76. doi: 10.1007/bf00211070.
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Antidiuretic hormone action in A6 cells: effect on apical Cl and Na conductances and synergism with aldosterone for NaCl reabsorption.

Verrey F .


Abstract
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-.

PubMed ID: 8189433
Article link: J Membr Biol


Species referenced: Xenopus laevis
Genes referenced: avp camp

References [+] :
Asher, Expression of the amiloride-blockable Na+ channel by RNA from control versus aldosterone-stimulated tissue. 1992, Pubmed, Xenbase