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1 Institut National de la Sante et de la Recherche Medicale Unite 356, Universite Rene Descartes, IFR 58, Paris, France
2 Institut National de la Sante et de la Recherche Medicale Unite 76, Institut National de la Transfusion Sanguine, Paris, France
3 Departement de Physiologie, Assistance Publique-Hopitaux de Paris, HEGP, Paris, France
4 Service de Biochimie, Assistance Publique-Hopitaux de Paris, HEGP, Paris, France
5 Institut National de la Sante et de la Recherche Medicale Unite 356, Universite Rene Descartes, IFR 58, Paris, France; Departement de Physiologie, Assistance Publique-Hopitaux de Paris, HEGP, Paris, France
6 Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA
* To whom correspondence should be addressed. E-mail: eladari{at}ccr.jussieu.fr.
Pendrin (Slc26A4) is a new anion exchanger that is believed to mediate apical Cl-/HCO3- exchange in 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 pendrin (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 semi-quantitative immunoblotting in renal membrane fractions isolated from the cortex of treated and control rats. We observed a consistent inverse relationship between pendrin expression and diet-induced changes in chloride excretion independent of the administered cation. Conversely, NaCl depletion induced by furosemide was associated with increased pendrin expression. We conclude that Pds expression is specifically regulated in response to changes in chloride balance.
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