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This Article Full Text Full Text (PDF) All Versions of this Article: 295/2/F497    most recent 00425.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Wang, G. Articles by Frøkiær, J. Search for Related Content PubMed PubMed Citation Articles by Wang, G. Articles by Frøkiær, J.

Ureter obstruction alters expression of renal acid-base transport proteins in rat kidney

¹The Water and Salt Research Center, ²Institute of Clinical Medicine, and ⁵Department of Cell Biology, Institute of Anatomy, University of Aarhus, Aarhus C; ³Department of Paediatric Surgery, 3rd Teaching Hospital and Institute of Clinical Medicine, Zhengzhou University, Henan, China; ⁴Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea; ⁶Department of Clinical Physiology, Aarhus University Hospital-Skejby, Aarhus N; and ⁷Department of Nephrology, Aarhus University Hospital-Aalborg, Aarhus, Denmark

Submitted 10 September 2007 ; accepted in final form 23 May 2008

Urinary tract obstruction impairs renal function and is often associated with a urinary acidification defect caused by diminished net H⁺ secretion and/or HCO₃^– reabsorption. To identify the molecular mechanisms of these defects, protein expression of key acid-base transporters were examined along the renal nephron and collecting duct of kidneys from rats subjected to 24-h bilateral ureteral obstruction (BUO), 4 days after release of BUO (BUO-R), or BUO-R rats with experimentally induced metabolic acidosis (BUO-A). Semiquantitative immunoblotting revealed that BUO caused a significant reduction in the expression of the type 3 Na⁺/H⁺ exchanger (NHE3) in the cortex (21 ± 4%), electrogenic Na⁺/HCO₃^– cotransporter (NBC1; 71 ± 5%), type 1 bumetanide-sensitive Na⁺-K⁺-2Cl^– cotransporter (NKCC2; 3 ± 1%), electroneutral Na⁺/HCO₃^– cotransporter (NBCn1; 46 ± 7%), and anion exchanger (pendrin; 87 ± 2%). The expression of H⁺-ATPase increased in the inner medullary collecting duct (152 ± 13%). These changes were confirmed by immunocytochemistry. In BUO-R rats, there was a persistent downregulation of all the acid-base transporters including H⁺-ATPase. Two days of NH₄Cl loading reduced plasma pH and HCO₃^– levels in BUO-A rats. The results demonstrate that the expression of multiple renal acid-base transporters are markedly altered in response to BUO, which may be responsible for development of metabolic acidosis and contribute to the urinary acidification defect after release of the obstruction.

ureteral obstruction; HCO₃^– reabsorption; urinary acidification defect