Antidiuretic hormone action in A6 cells: effect on apical Cl and Na conductances and synergism with aldosterone for NaCl reabsorption.
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-.
Verrey
F
F
Institute of Physiology, University of Zürich, Switzerland.
D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000450:Aldosterone / Q000502:physiology*; D000818:Animals; D001692:Biological Transport; D002034:Bumetanide / Q000494:pharmacology; D002460:Cell Line; D002712:Chlorides / Q000378:metabolism / Q000502:physiology*; D005576:Colforsin / Q000494:pharmacology; D007454:Iodides / Q000378:metabolism; D007668:Kidney / Q000166:cytology / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D012964:Sodium / Q000502:physiology*; D012965:Sodium Chloride / Q000378:metabolism*; D014667:Vasopressins / Q000502:physiology*; D014668:Vasotocin / Q000502:physiology; D014982:Xenopus laevis
D002712:Chlorides; D007454:Iodides; D002034:Bumetanide; D014667:Vasopressins; D005576:Colforsin; D015124:8-Bromo Cyclic Adenosine Monophosphate; D012965:Sodium Chloride; D000450:Aldosterone; D012964:Sodium; D014668:Vasotocin