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Dietary Cl^– restriction upregulates pendrin expression within the apical plasma membrane of type B intercalated cells

¹Department of Medicine, University of Florida College of Medicine, Gainesville, Florida; ²Department of Medicine, Emory University, Atlanta, Georgia; ³Department of Medicine, University of Texas, Health Science Center at Houston, Houston, Texas; ⁴Hypertension and Vascular Research Division, Henry Ford Hospital and Wayne State School of Medicine, Detroit, Michigan; ⁵Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland; and ⁶The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Cambridge, United Kingdom

Submitted 29 November 2005 ; accepted in final form 3 April 2006

Pendrin, encoded by Slc26a4, is a Cl^–/HCO₃^– exchanger expressed in the apical region of type B and non-A, non-B intercalated cells, which regulates renal NaCl excretion. Dietary Cl^– restriction upregulates total pendrin protein expression. Whether the subcellular expression of pendrin and whether the apparent vascular volume contraction observed in Slc26a4 null mice are Cl^– dependent, but Na⁺ independent, is unknown. Thus the subcellular distribution of pendrin and its role in acid-base and fluid balance were explored using immunogold cytochemistry and balance studies of mice ingesting a NaCl-replete or a Na⁺-replete, Cl^–-restricted diet, achieved through substitution of NaCl with NaHCO₃. Boundary length and apical plasma membrane pendrin label density each increased by 60–70% in type B intercalated cells, but not in non-A, non-B cells, whereas cytoplasmic pendrin immunolabel increased 60% in non-A, non-B intercalated cells, but not in type B cells. Following either NaCl restriction or Cl^– restriction alone, Slc26a4 null mice excreted more Cl^– and had a higher arterial pH than pair-fed wild-type mice. In conclusion, 1) following dietary Cl^– restriction, apical plasma membrane pendrin immunolabel increases in type B intercalated cells, but not in non-A, non-B intercalated cells; and 2) pendrin participates in the regulation of renal Cl^– excretion and arterial pH during dietary Cl^– restriction.

acid-base and fluid balance; mammalian collecting duct

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