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Intercalated cell H⁺/OH^– transporter expression is reduced in Slc26a4 null mice

¹Department of Medicine, Emory University, Atlanta, Georgia; ²Department of Medicine, University of Florida College of Medicine, Gainesville, Florida; ⁵The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom; ⁶Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland; ⁷The Water and Salt Research Center, Aarhus University, Aarhus, Denmark; ³Division of Nephrology, University California School of Medicine, Los Angeles, California; and ⁴Nephrology and Hypertension Section, North Florida/South Georgia Veterans Health System, Gainesville, Georgia

Submitted 18 May 2005 ; accepted in final form 9 August 2005

Slc26a4 (Pds) encodes pendrin, a Cl^–/HCO₃^– exchanger expressed in the apical region of type B and non-A, non-B cells, which mediates secretion of OH^– equivalents. Thus genetic disruption of Slc26a4 leads to systemic alkalosis in some treatment models. However, humans and mice with genetic disruption of Slc26a4 have normal acid-base balance under basal conditions. Thus we asked: 1) Is net acid excretion altered in Slc26a4 (–/–) mice under basal conditions? 2) In the absence of pendrin-mediated OH^– secretion, are increases in intracellular and systemic pH minimized through changes in intercalated cell subtype abundance or intercalated cell H⁺/OH^– transporter expression? To answer these questions, net acid excretion and H⁺/OH^– transporter expression were examined in Slc26a4 (–/–) and Slc26a4 (+/+) mice using balance studies, immunolocalization, and immunoblotting. Excretion of ammonium, titratable acid, and citrate were the same in Slc26a4 null and wild-type mice. However, urinary pH and PCO₂ were much lower in Slc26a4 null relative to wild-type mice due to reduced urinary buffering of secreted H⁺ by HCO₃^–. Abundance of non-A, but not type A intercalated cells, was reduced within the cortical collecting ducts of Slc26a4 null mice. Moreover, kidneys from Slc26a4 null mice had reduced H⁺-ATPase, NBC3 and RhBG total protein expression, particularly within type B and non-A, non-B intercalated cells, although RhCG protein expression was unchanged. Reduced intercalated cell H⁺/OH^– transporter expression is observed in Slc26a4 null mice, which likely attenuates the rise in intracellular and systemic pH expected with genetic disruption of Slc26a4.

NBC3; AE1; acid-base balance

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