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Am J Physiol Renal Physiol 287: F1179-F1188, 2004. First published August 3, 2004; doi:10.1152/ajprenal.00211.2004
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The Cl–/HCO3– exchanger pendrin in the rat kidney is regulated in response to chronic alterations in chloride balance

Fabienne Quentin,1 Régine Chambrey,1 Marie Marcelle Trinh-Trang-Tan,2 Marinos Fysekidis,3 Michèle Cambillau,4 Michel Paillard,1,3 Peter S. Aronson,5 and Dominique Eladari1,3

1Institut National de la Santé et de la Recherche Médicale Unité 356, Institut Fédératif de Recherche 58, Université René Descartes, 75006 Paris; 2Institut National de la Santé et de la Recherche Médicale Unité 76, Institut National de la Transfusion Sanguine, and 3Département de Physiologie and 4Service de Biochimie, Hôpital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, 75015 Paris, France; and 5Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8029

Submitted 7 June 2004 ; accepted in final form 28 July 2004

Pendrin (Pds; Slc26A4) is a new anion exchanger that is believed to mediate apical Cl–/HCO3– exchange in type B and non-A-non-B intercalated cells of the connecting tubule and cortical collecting duct. Recently, it has been proposed that this transporter may be involved in NaCl balance and blood pressure regulation in addition to its participation in the regulation of acid-base status. The purpose of our study was to determine the regulation of Pds protein abundance during chronic changes in chloride balance. Rats were subjected to either NaCl, NH4Cl, NaHCO3, KCl, or KHCO3 loading for 6 days or to a low-NaCl diet or chronic furosemide administration. Pds protein abundance was estimated by semiquantitative immunoblotting in renal membrane fractions isolated from the cortex of treated and control rats. We observed a consistent inverse relationship between Pds expression and diet-induced changes in chloride excretion independent of the administered cation. Conversely, NaCl depletion induced by furosemide was associated with increased Pds expression. We conclude that Pds expression is specifically regulated in response to changes in chloride balance.

anion exchanger; extracellular volume; blood pressure; HTA; acid-base


Address for reprint requests and other correspondence: D. Eladari and R. Chambrey, Unité INSERM 356, Institut de Recherche des Cordeliers, 15 rue de l'Ecole de Médecine, 75270 Paris Cedex 06, France (E-mail: eladari{at}ccr.jussieu.fr and chambrey{at}ccr.jussieu.fr)




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