Aldosterone stimulates intestinal Na+ absorption in rats by increasing NHE3 expression of the proximal colon

Judy H. Cho, Mark W. Musch, Crescence M. Bookstein, Rebecca L. McSwine, Karen Rabenau, Eugene B. Chang

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

Abstract

Na+ retention by the colon in response to salt deprivation is mediated in part by the resulting secondary hyperaldosteronism. We show that experimental hyperaldosteronism, to levels seen with salt deprivation, causes an increase in the selective expression and activity of NHE3, an apically located isoform of the Na+/H+ exchange family that functions in transepithelial Na+ absorption. The effect of aldosterone on NHE3 expression is tissue specific, occurring in intestine and not in kidney. Within the intestine, these effects are regional, being observed only in proximal colon, and different in distribution from that observed with glucocorticoids, where the predominant effect occurs in ileum. Although glucocorticoids are well known to exert many effects via regulation of transcript levels, the present study demonstrates that aldosterone stimulates intestinal Na+ absorption by increasing cellular NHE3 expression, a response that is tissue and region specific.

Original languageEnglish
Pages (from-to)C586-C594
JournalAmerican Journal of Physiology - Cell Physiology
Volume274
Issue number3 43-3
DOIs
StatePublished - Mar 1998
Externally publishedYes

Keywords

  • Fluid and electrolyte transport
  • Gene regulation
  • Intestine
  • Kidney
  • Mineralocorticoids
  • Sodium absorption
  • Sodium/hydrogen antiporter
  • Sodium/hydrogen exchanger isoform 3

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