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NDT Advance Access originally published online on September 5, 2007
Nephrology Dialysis Transplantation 2007 22(12):3462-3470; doi:10.1093/ndt/gfm486
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© The Author [2007].
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org


Regulation of the basolateral chloride/base exchangers AE1 and SLC26A7 in the kidney collecting duct in potassium depletion

Sharon Barone1, Hassane Amlal1, Minna Kujala2, Jie Xu1, Fiona Karet3, Ann Blanchard4, Juha Kere5 and Manoocher Soleimani1,6

1Department of Medicine, University of Cincinnati, Cincinnati, OH, USA, 2Medical Genetics, University of Helsinki, Finland, 3Department of Medical Genetics and Division of Renal Medicine, University of Cambridge, Cambridge, UK, 4Université Paris Descartes, faculté de médecine, Paris, France, 5Biosciences at Novum, Karolinska Institute, Huddinge Sweden and 6Research Services, Veterans Affairs Medical Center at Cincinnati, OH, USA

Correspondence to: M. Soleimani, MD, Department of Medicine, University of Cincinnati, 231 Albert Sabin Way, MSB G259, Cincinnati, OH 45267-0585, USA. Email: manoocher.soleimani{at}uc.edu



  Abstract

In the present study, the effect of potassium depletion on the expression of acid-base transporters in the collecting duct was examined. Toward this end rats were fed a potassium-free diet for 3 weeks. Thereafter, the expression of the basolateral chloride/bicarbonate exchangers AE1 and SLC26A7 and the apical H+-ATPase was examined by northern hybridization, immunoblot analysis and immunofluorescence labelling. The mRNA expression of AE1 increased by a robust ~500% in the cortex and ~70% in the outer medulla, which translated into a huge increase in AE1 protein abundance in the cortex and a moderate increase in the outer medulla in K-depletion. The mRNA expression of SLC26A7 did not change significantly but its protein abundance showed a robust increase in the outer medulla. The expression of SLC26A7 remained undetected in the cortex in K-depleted rats. The post translational increase in SLC26A7 membrane abundance in potassium depletion was recapitulated in vitro using epitope-tagged SLC26A7. H+-ATPase displayed enhanced apical plasma membrane immunoreactivity in the OMCD in K-depletion. We suggest that the up-regulation of SLC26A7 and AE1 on the basolateral membrane of A-intercalated cells in the OMCD and CCD, respectively, along with H+-ATPase on the apical membrane, contributes to enhanced bicarbonate absorption in the collecting duct in K-depletion.

Keywords: bicarbonate absorption; kidney tubules; metabolic alkalosis

Received for publication: 27. 3.07
Accepted in revised form: 26. 6.07


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