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Articles in PresS, published online ahead of print October 22, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00254.2002
Submitted on July 15, 2002
Accepted on October 10, 2002
1 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Anatomy, University of Aarhus, Aarhus, Denmark
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Physiology, School of Medicine, Dongguk University, Kyungju, Korea, Republic of
3 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Experimental Clinical Research, University of Aarhus, Aarhus, Denmark
4 Department of Medicine, University of Florida, Gainesville, Florida, USA
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
The anion exchanger pendrin is present in the apical plasma membrane of type B and nonA-nonB intercalated cells of the cortical collecting duct (CCD) and connecting tubule (CNT) and is involved in bicarbonate 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 mmoles NH4Cl/g bw for 7 days) dramatically reduced pendrin abundance to 22 ± 4 % of controls (n = 6, P < 0.005). Immunoperoxidase labeling for pendrin showed reduced intensity in NH4Cl-loaded animals compared to controls. Moreover, double labeling 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 mmoles NaHCO3/g bw for 7 days) induced a significant increase in pendrin expression to 153 ± 11 % of controls (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 intracellular vesicles in all conditions. These results indicate that changes in pendrin protein expression play a key role in the well established regulation of bicarbonate 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.
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