Cellular Physiology and Biochemistry
Review
Regulation of Extracellular Fluid Volume and Blood Pressure by PendrinHadchouel J.1,2 · Büsst C.1,2 · Procino G.3 · Valenti G.3 · Chambrey R.4,5 · Eladari D.4,5,61INSERM UMRS 970 - Paris Cardiovascular Research Center (PARCC) and2University Paris-Descartes, Paris,3Department of General and Environmental Physiology, University of Bary, Bari,4Centre de Recherche des Cordeliers, Université Paris Descartes, INSERM UMRS 872, Equipe 3, and5Université Pierre et Marie Curie, CNRS ERI 7226, Paris,6Department of Physiology, Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Paris
Dominique Eladari Centre de Recherche des Cordeliers, Equipe 3, 15, rue de l’Ecole de Médecine, F-75270 Paris Cedex 06 (France) Tel. +33 1 55 42 78 63, Fax + 33 1 46 33 41 72 E-Mail dominique.eladari&commat crc.jussieu.fr |
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Abstract
Na+ is commonly designed as the culprit of salt-sensitive hypertension but several studies suggest that abnormal Cl- transport is in fact the triggering mechanism. This review focuses on the regulation of blood pressure (BP) by pendrin, an apical Cl-/HCO3- exchanger which mediates HCO3- secretion and transcellular Cl- transport in type B intercalated cells (B-ICs) of the distal nephron. Studies in mice showed that it is required not only for acid-base regulation but also for BP regulation as pendrin knock-out mice develop hypotension when submitted to NaCl restriction and are resistant to aldosterone-induced hypertension. Pendrin contributes to these processes by two mechanisms. First, pendrin-mediated Cl- transport is coupled with Na+ reabsorption by the Na+-dependent Cl-/HCO3- exchanger NDCBE to mediate NaCl reabsorption in B-ICs. Second, pendrin activity regulates Na+ reabsorption by the adjacent principal cells, possibly by interaction with the ATP-mediated paracrine signalling recently identified between ICs and principal cells. Interestingly, the water channel AQP5 was recently found to be expressed at the apical side of B-ICs, in the absence of a basolateral water channel, and pendrin and AQP5 membrane expressions are both inhibited by K+ depletion, suggesting that pendrin and AQP5 could cooperate to regulate cell volume, a potent stimulus of ATP release.
© 2011 S. Karger AG, Basel
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Article / Publication Details
Accepted: October 06, 2011
Published online: November 18, 2011
Issue release date: November 2011
Number of Print Pages: 8
Number of Figures: 0
Number of Tables: 0
ISSN: 1015-8987 (Print)
eISSN: 1421-9778 (Online)
For additional information: https://www.karger.com/CPB
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