First Author | Verlander JW | Year | 2006 |
Journal | Am J Physiol Renal Physiol | Volume | 291 |
Issue | 4 | Pages | F833-9 |
PubMed ID | 16670435 | Mgi Jnum | J:112416 |
Mgi Id | MGI:3656314 | Doi | 10.1152/ajprenal.00474.2005 |
Citation | Verlander JW, et al. (2006) Dietary Cl- restriction upregulates pendrin expression within the apical plasma membrane of type B intercalated cells. Am J Physiol Renal Physiol 291(4):F833-9 |
abstractText | 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. |