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1 INSERM U652, IFR58, Institut des Cordeliers, Universite Rene Descartes, Paris, 75006, France
2 INSERM U665, Institut National de la Transfusion Sanguine, Paris, 75015, France
3 UMR 7134, CNRS-Universite Pierre et Marie Curie, Paris, 75006, France
4 INSERM U652, IFR58, Institut des Cordeliers, Universite Rene Descartes, Paris, 75006, France; Departement de Physiologie, Hopital Europeen Georges Pompidou, AP-HP, Paris, 75015, France
5 INSERM U439, Hopital Lariboisiere, Paris, 75010, France
6 Service de Biochimie, Hopital Europeen Georges Pompidou, AP-HP, Paris, 75015, France
7 INSERM U652, IFR58, Institut des Cordeliers, Universite Rene Descartes, Paris, 75006, France; Departement de Physiologie, Hopital Necker-Enfant Malades, AP-HP, Paris, 75015, France
* To whom correspondence should be addressed. E-mail: chambrey{at}ccr.jussieu.fr.
Ammonium transport by the distal nephron and ammonium detoxification by the liver, are critical for achieving regulation of acid-base balance and to avoid hyperammonemic hepatic encephalopathy, respectively. Therefore, it has been proposed that Rhbg, a member of the Mep/Amt/Rh ammonia channel superfamily, may be involved in some forms of distal tubular acidosis and congenital hyperammonemia. We have tested this hypothesis by inactivating RHbg gene in mouse by insertional mutagenesis. Histochemical studies analyses confirmed that RHbg KO mice did not express Rhbg protein. Under basal conditions, the KO mice did not exhibit encephalopathy and survived well. They did not exhibit hallmarks of distal tubular acidosis since neither acid-base status, serum potassium concentration, nor bone mineral density were altered by RHbg disruption. They did not have hyperammonemia or disturbed hepatic ammonia metabolism. Moreover, the KO mice adapted to a chronic acid-loading challenge by increasing urinary ammonium excretion as well as their wild type controls. Finally, transepithelial NH3 diffusive permeability, or NH3 and NH4 + entry across the basolateral membrane of cortical collecting duct cells, measured by in vitro microperfusion of collecting duct from KO and wild type mice were identical with no apparent effect of the absence of Rhbg protein. We conclude that Rhbg is not a critical determinant of ammonium excretion by the kidney and of ammonium detoxification by the liver in vivo.
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