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Articles in PresS, published online ahead of print August 13, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00205.2002
Submitted on May 30, 2002
Accepted on August 13, 2002
1 Research Services, Veterans Affairs Medical Center, Cincinnati, OH, USA; Department of Medicine, University of Cincinnati, Cincinnati, OH, USA
2 Department of Medicine, University of Cincinnati, Cincinnati, OH, USA
3 Research Services, Veterans Affairs Medical Center, Cincinnati, OH, USA
4 Department of Medicine, University of Cincinnati, Cincinnati, OH, USA; Research Services, Veterans Affairs Medical Center, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: manoocher.soleimani{at}uc.edu.
Pendrin is an apical Cl-/OH-/HCO3- exchanger in ß-intercalated cells (ß-ICs) of rat and mouse cortical collecting duct (CCD). However, little is known about its regulation in acid-base disorders. Here, we examined the regulation of pendrin in metabolic acidosis, a condition known to decrease bicarbonate secretion in CCD. Rats were subjected to NH4Cl loading for 4 days, which resulted in metabolic acidosis. Apical Cl-/HCO3- exchanger activity in ß-ICs was determined as amplitude and rate of intracellular pH change upon chloride removal in isolated, microperfused CCDs. Intracellular pH was measured by single cell digital ratiometric imaging using fluorescent pH-sensitive dye BCPCF-AM. Pendrin mRNA expression in kidney cortex was examined by Northern hybridizations. Expression of pendrin protein was assessed by indirect immunofluorescence. Microperfused CCDs isolated from acidotic rats demonstrated ~60% reduction in apical Cl-/HCO3- exchanger activity in ß-ICs (p<0.001 vs. control). Northern hybridizations indicated that the mRNA expression of pendrin in kidney cortex decreased by 68% in acidotic animals (p<0.02 vs. control). Immunofluorescence labeling demonstrated significant reduction in pendrin expression in CCDs of acidotic rats. We conclude that metabolic acidosis decreases the activity of the apical Cl-/HCO3- exchanger in ß-ICs of the rat CCD by reducing the expression of pendrin. Adaptive downregulation of pendrin in metabolic acidosis indicates the important role of this exchanger in acid-base regulation in the CCD.
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