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

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...