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Short‐Term Aldosterone Action on Na,K‐ATPase Surface Expression
Author(s) -
VERREY FRANÇOIS,
SUMMA VANESSA,
HEITZMANN DIRK,
MORDASINI DAVID,
VANDEWALLE ALAIN,
FERAILLE ERIC,
ZECEVIC MARIJA
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2003.tb07253.x
Subject(s) - aldosterone , epithelial sodium channel , sgk1 , reabsorption , medicine , endocrinology , chemistry , downregulation and upregulation , renal sodium reabsorption , xenopus , ion transporter , microbiology and biotechnology , biology , sodium , glucocorticoid , kidney , biochemistry , organic chemistry , membrane , gene
A bstract : Aldosterone controls extracellular volume and blood pressure by regulating Na + reabsorption across epithelial cells of the aldosterone‐sensitive distal nephron (ASDN). This effect is mediated by a coordinate action on the luminal channel ENaC (generally rate limiting) and the basolateral Na,K‐ATPase. Long‐term effects of aldosterone (starting within 3 to 6 hours and increasing over days) are mediated by the direct and indirect induction of stable elements of the Na + transport machinery (e.g., Na,K‐ATPase α subunit), whereas short‐term effects appear to be mediated by the upregulation of short‐lived elements of the machinery (e.g., ENaC α subunit) and of regulatory proteins, such as the serum‐ and glucocorticoid‐regulated kinase SGK1. We have recently shown that in cortical collecting duct (CCD) from adrenalectomized (ADX) rats, the increase in Na,K‐ATPase activity (approximately threefold in 3 h), induced by a single aldosterone injection, can be fully accounted for by the increase in Na,K‐ATPase cell‐surface expression. Using the model cell line mpkCCD cl4 , we showed that the parallel increase in Na,K‐ATPase function [assessed by Na + pump current (I p ) measurements] and cell‐surface expression depends on transcription and translation, and that it is not secondary to a change in apical Na + influx. As a first approach to address the question whether the aldosterone‐induced regulatory protein SGK1 might play a role in mediating Na,K‐ATPase translocation, we have used the Xenopus laevis expression system. SGK1 coexpression indeed increased both the Na + pump current and the surface expression of pumps containing the rat α1 subunits. In summary, aldosterone controls Na + reabsorption in the short term not only by regulating the apical cell‐surface expression of ENaC but also by coordinately acting on the basolateral cell‐surface expression of the Na,K‐ATPase. Results obtained in the Xenopus oocyte expression system suggest the possibility that this effect could be mediated in part by the aldosterone‐induced kinase SGK1.