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

2006; American Physical Society; Volume: 291; Issue: 4 Linguagem: Inglês

10.1152/ajprenal.00474.2005

1931-857X

Jill W. Verlander, Young Hee Kim, Wonkyong Shin, Truyen D. Pham, Kathryn A. Hassell, William H. Beierwaltes, Eric D. Green, Lorraine A. Everett, Sharon W. Matthews, Susan M. Wall,

Sodium Intake and Health

Pendrin, encoded by Slc26a4, is a Cl(-)/HCO(3)(-) 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 NaHCO(3). Boundary length and apical plasma membrane pendrin label density each increased by approximately 60-70% in type B intercalated cells, but not in non-A, non-B cells, whereas cytoplasmic pendrin immunolabel increased approximately 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.