Chronic metabolic acidosis increases NaDC-1 mRNA and protein abundance in rat kidney

Seiji Aruga, Stephan Wehrli, Brigitte Kaissling, Orson W. Moe, Patricia A. Preisig, Ana M. Pajor, Robert J. Alpern

Research output: Contribution to journalArticle

89 Scopus citations

Abstract

Background: Chronic metabolic acidosis increases, while alkali feeding inhibits, proximal tubule citrate absorption. The activity of the apical membrane Na+/citrate cotransporter is increased in metabolic acidosis, but is not altered by alkali feeding. Methods: Renal cortical mRNA and brush border membrane protein abundances of sodium/dicarboxylate-1 (NaDC-1), the apical membrane Na+/citrate transporter, were measured. Results: By immunohistochemistry, NaDC-1 was localized to the apical membrane of the proximal tubule. Chronic metabolic acidosis caused an increase in NaDC-1 protein abundance that was maximal in the S2 segment and that increased with time. Metabolic acidosis also increased NaDC-1 mRNA abundance, but this was first seen at three hours and correlated with the severity of the metabolic acidosis. Alkali feeding had no effect on NaDC-1 protein or mRNA abundance. Conclusions: Chronic metabolic acidosis increases renal cortical NaDC-1 mRNA abundance and apical membrane NaDC-1 protein abundance, while alkali feeding is without effect on NaDC-1.

Original languageEnglish (US)
Pages (from-to)206-215
Number of pages10
JournalKidney international
Volume58
Issue number1
DOIs
StatePublished - Jan 1 2000

Keywords

  • Alkali feeding
  • Citrate
  • Hypercitrituria
  • Proximal tubule
  • Sodium/dicarboxylate cotransport

ASJC Scopus subject areas

  • Nephrology

Fingerprint Dive into the research topics of 'Chronic metabolic acidosis increases NaDC-1 mRNA and protein abundance in rat kidney'. Together they form a unique fingerprint.

  • Cite this

    Aruga, S., Wehrli, S., Kaissling, B., Moe, O. W., Preisig, P. A., Pajor, A. M., & Alpern, R. J. (2000). Chronic metabolic acidosis increases NaDC-1 mRNA and protein abundance in rat kidney. Kidney international, 58(1), 206-215. https://doi.org/10.1046/j.1523-1755.2000.00155.x