Effect of glucocorticoids on renal cortical NHE-3 and NHE-1 mRNA

Michel Baum, Orson W. Moe, Danny L. Gentry, Robert J. Alpern

Research output: Contribution to journalArticlepeer-review

12 Scopus citations


Glucocorticoids play an important role in modulating proximal tubule acidification. Chronic systemic administration of dexamethasone increases the rate of bicarbonate absorption in isolated perfused proximal convoluted tubules and Na+/H+ antiporter activity in renal brush-border membrane vesicles. The proximal tubule expresses mRNA corresponding to two known Na+/H+ antiporter isoforms: NHE-3, an amiloride-resistant apical membrane Na+/H+ antiporter; and NHE-1, an amiloride-sensitive Na+/H+ antiporter found on most mammalian cells. Administration of dexamethasone for 1 and 2 days (600 μg/kg twice daily and 2 h before animals were killed) increased NHE-3 mRNA abundance 1.3- and 2.5-fold, respectively, but had no effect on NHE-1 mRNA abundance. Aminoglutethimide-induced glucocorticoid deficiency had no effect on NHE-1 or NHE-3 mRNA abundance. Incubation of proximal tubules for 3 h with 10-5 M dexamethasone increased proximal tubule Na+/H+ antiporter activity from 0.69 ± 0.04 to 0.92 ± 0.03 pH units/min (P < 0.01); however, there was no increase in NHE-3 or NHE-1 mRNA abundance. Similarly, there was no effect on NHE-3 or NHE-1 mRNA abundance in rabbit renal cortex 4 h after intravenous administration of 600 μg/kg dexamethasone. Thus chronic dexamethasone increases NHE-3 but not NHE-1 mRNA abundance. The acute increase in Na+/H+ antiporter activity induced by dexamethasone occurs by mechanisms independent of changes in NHE-1 and NHE-3 mRNA abundance.

Original languageEnglish (US)
Pages (from-to)F437-F442
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number3 36-3
StatePublished - 1994


  • acidification
  • dexamethasone
  • sodium-hydrogen antiporter

ASJC Scopus subject areas

  • Physiology


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