In:
American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 295, No. 2 ( 2008-08), p. F497-F506
Abstract:
Urinary tract obstruction impairs renal function and is often associated with a urinary acidification defect caused by diminished net H + secretion and/or HCO 3 − 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 + /HCO 3 − cotransporter (NBC1; 71 ± 5%), type 1 bumetanide-sensitive Na + -K + -2Cl − cotransporter (NKCC2; 3 ± 1%), electroneutral Na + /HCO 3 − 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 NH 4 Cl loading reduced plasma pH and HCO 3 − 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.
Type of Medium:
Online Resource
ISSN:
1931-857X
,
1522-1466
DOI:
10.1152/ajprenal.00425.2007
Language:
English
Publisher:
American Physiological Society
Publication Date:
2008
detail.hit.zdb_id:
1477287-5
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