Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule.

Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule. Research Abstract Details 

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Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule. Abstract Text:

Snezana Petrovic,Sharon Barone,Zhaohui Wang,Alicia A McDonough,Hassane Amlal,Manoocher Soleimani,Snezana Petrovic,Sharon Barone,Zhaohui Wang,Alicia A McDonough,Hassane Amlal,Manoocher Soleimani,

BACKGROUND/AIM: Slc26a6 (PAT1, CFEX) is a major chloride/base exchanger located on the apical membrane of the kidney proximal tubule. The purpose of the present study was to examine the effect of Slc26a6 deletion on the apical Na+/H+ exchanger 3 (NHE3) in the straight segment (S3) of the proximal tubule, which is the major site for the reabsorption of filtered chloride in the kidney. METHODS: The proximal tubule S3 segment was perfused and the intracellular pH and apical Na+/H+ exchanger activity and expression were measured. RESULTS: In the proximal tubule straight segments that were microperfused in vitro, baseline intracellular pH, measured by BCPCF-AM, was 7.10 +/- 0.02 in Slc26a6-/- and 7.33 +/- 0.02 in Slc26a6+/+ animals, a significant reduction in Slc26a6 mutant mice (p < 0.00001). The activity of the apical Na+/H+ exchanger was 0.49 +/- 0.02 pH units/min in Slc26a6+/+ and 0.26 +/- 0.03 pH units/min in Slc26a6-/- animals, a significant reduction in Slc26a6-/- mice (p < 0.0001). Formate-induced intracellular alkalinization, which is mediated via NHE3, was significantly blunted in Slc26a6-/- animals, with an alkalinization magnitude of 0.16 pH unit in Slc26a6-/- versus 0.37 in Slc26a6+/+ animals (p < 0.00001, n = 5 separate animals). Angiotensin II stimulation of NHE3 activity was intact in Slc26a6-/- animals. Buffering capacity was comparable in Slc26a6+/+ and Slc26a6-/- mice. Immunoblotting and immunofluorescent labeling demonstrated comparable NHE3 abundance and distribution in kidney proximal tubules of Slc26a6+/+ and Slc26a6-/- mice. CONCLUSION: In conclusion, Slc26a6 deletion downregulates the apical Na+/H+ exchanger activity in the straight segment of the proximal tubule. The absence of a significant renal sodium loss in Slc26a6-null mice, despite NHE3 downregulation in the in vitro perfused tubules, points to possible activation of signaling pathways that can stimulate the apical Na+/H+ exchanger in vivo.

Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule. Publishing Authors By Initials

S Petrovic,S Barone,Z Wang,AA McDonough,H Amlal,M Soleimani,S Petrovic,S Barone,Z Wang,AA McDonough,H Amlal,M Soleimani,

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Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule. Journal Published:

PUBLICATION TYPE: Research Support, U.S. Gov't,

Journal: American journal of nephrology

VOLUME: 28

Page Numbers: 330-8

Journal Abbreviation: Am. J. Nephrol.

ISSN: 1421-9670

DAY: 29

MONTH: 11

YEAR: 2007

Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Slc26a6 (PAT1) deletion downregulates the apical Na+/H+ exchanger in the straight segment of the proximal tubule.

AFFILIATION: Department of Medicine, University of Cincinnati, Cincinnati, Ohio 45267-0585, USA.

Country: Switzerland

AGENCY: United States NIDDK

GRANT: DK 62809

ACRONYM: DK

MEDLINETA: Am J Nephrol

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