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Am J Physiol Renal Physiol 284: F584-F593, 2003. First published October 22, 2002; doi:10.1152/ajprenal.00254.2002
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Vol. 284, Issue 3, F584-F593, March 2003

Regulated expression of pendrin in rat kidney in response to chronic NH4Cl or NaHCO3 loading

Sebastian Frische1,2, Tae-Hwan Kwon1,3, Jørgen Frøkiær1,4, Kirsten M. Madsen5, and Søren Nielsen1,2

1 The Water and Salt Research Center, 2 Institute of Anatomy, and 4 Institute of Experimental Clinical Research, University of Aarhus, DK-8000 Aarhus C, Denmark; 3 Department of Physiology, School of Medicine, Dongguk University, 780-714 Kyungju, Korea; and 5 Department of Medicine, University of Florida, Gainesville, Florida

The anion exchanger pendrin is present in the apical plasma membrane of type B and non-A-non-B intercalated cells of the cortical collecting duct (CCD) and connecting tubule and is involved in HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> secretion. In this study, we investigated whether the abundance and subcellular localization of pendrin are regulated in response to experimental metabolic acidosis and alkalosis with maintained water and sodium intake. NH4Cl loading (0.033 mmol NH4Cl/g body wt for 7 days) dramatically reduced pendrin abundance to 22 ± 4% of control values (n = 6, P < 0.005). Immunoperoxidase labeling for pendrin showed reduced intensity in NH4Cl-loaded animals compared with control animals. Moreover, double-label laser confocal microscopy revealed a reduction in the fraction of cells in the CCD exhibiting pendrin labeling to 65% of the control value (n = 6, P < 0.005). Conversely, NaHCO3 loading (0.033 mmol NaHCO3/g body wt for 7 days) induced a significant increase in pendrin expression to 153 ± 11% of control values (n = 6, P < 0.01) with no change in the fraction of cells expressing pendrin. Immunoelectron microscopy revealed no major changes in the subcellular distribution, with abundant labeling in both the apical plasma membrane and the intracellular vesicles in all conditions. These results indicate that changes in pendrin protein expression play a key role in the well-established regulation of HCO<UP><SUB>3</SUB><SUP>−</SUP></UP> secretion in the CCD in response to chronic changes in acid-base balance and suggest that regulation of pendrin expression may be clinically important in the correction of acid-base disturbances.

collecting duct; acid-base balance; intercalated cells; electron microscopy; immunocytochemistry


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