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Pendrin Regulation in Mouse Kidney Primarily Is Chloride-Dependent

Marion Vallet^*,, Nicolas Picard^*,, Dominique Loffing-Cueni, Marinos Fysekidis^*,, May Bloch-Faure, Georges Deschênes, Sylvie Breton^||, Pierre Meneton^*,, Johannes Loffing, Peter S. Aronson^¶, Régine Chambrey^*, and Dominique Eladari^*,,**

^* INSERM U652, IFR58, Institut des Cordeliers; Université Paris-Descartes, Faculté de Médecine René Descartes; UMR 7134 CNRS-Université Pierre et Marie Curie; ^** Département de Physiologie, Hôpital Necker-Enfant Malades, AP-HP, Paris, France; University of Fribourg, Department of Medicine, Unit of Anatomy, Fribourg, Switzerland; ^|| Program in Membrane Biology, Massachusetts General Hospital, and Department of Medicine, Harvard Medical School, Boston, Massachusetts; and ^¶ Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut

Address correspondence to: Dr. Régine Chambrey or Dr. Dominique Eladari, INSERM U652, IFR58, Institut des Cordeliers, 15 rue de l’Ecole de médecine, 75006 Paris, France. Phone: +33-1-4441-3718; Fax: +33-1-4441-3717; E-mail: chambrey{at}ccr.jussieu.fr or eladari@ccr.jussieu.fr

Received for publication October 12, 2005. Accepted for publication May 21, 2006.

Recent studies indicate that pendrin, an apical Cl^–/HCO₃^– exchanger, mediates chloride reabsorption in the connecting tubule and the cortical collecting duct and therefore is involved in extracellular fluid volume regulation. The purpose of this study was to test whether pendrin is regulated in vivo primarily by factors that are associated with changes in renal chloride transport, by aldosterone, or by the combination of both determinants. For achievement of this goal, pendrin protein abundance was studied by semiquantitative immunoblotting in different mouse models with altered aldosterone secretion or tubular chloride transport, including NaCl loading, hydrochlorothiazide administration, NaCl co-transporter knockout mice, and mice with Liddle’s mutation. The parallel regulation of the aldosterone-regulated epithelial sodium channel (ENaC) was examined as a control for biologic effects of aldosterone. Major changes in pendrin protein expression were found in experimental models that are associated with altered renal chloride transport, whereas no significant changes were detected in pendrin protein abundance in models with altered aldosterone secretion. Moreover, in response to hydrochlorothiazide administration, pendrin was downregulated despite a marked secondary hyperaldosteronism. In contrast, -ENaC was markedly upregulated, and the molecular weight of a large fraction of -ENaC subunits was shifted from 85 to 70 kD, consistent with previous results from rat models with elevated plasma aldosterone levels. These results suggest that factors that are associated with changes in distal chloride delivery govern pendrin expression in the connecting tubule and cortical collecting duct.

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