The lumen of the inner ear has an unusually-low concentration of endolymphatic Na⁺, which is important for the transduction processes. We have recently shown that glucocorticoid receptors (GR) stimulate absorption of Na⁺ by semicircular canal duct (SCCD) epithelia. In the current study, we sought to determine the presence of genes involved in control of the amiloride-sensitive Na⁺ transport pathway in rat SCCD epithelia and whether their level of expression was regulated by glucocorticoids using quantitative real-time RT-PCR. Transcripts were present for , & subunits of ENaC; ₁, ₃, ₁, & ₃ isoforms of Na⁺,K⁺-ATPase; inwardly rectifying potassium channels (Kir [IC₅₀ of short circuit current ((I_sc)) for Ba²⁺: 210 µM]) Kir2.1, Kir2.2, Kir2.3, Kir2.4, Kir3.1, Kir3.3, Kir4.1, Kir4.2, Kir5.1 & Kir7.1; sulfonyl urea receptor1 (SUR1); GR; mineralocorticoid receptor (MR); 11-hydroxysteroid dehydrogenase type1 ((11-HSD1)) & 11-HSD2; Sgk1 and Nedd4-2. On the other hand, transcripts for ₄-Na⁺,K⁺-ATPase; Kir1.1, Kir3.2 & Kir3.4, Kir6.1, Kir6.2 and SUR2 were found to be absent and I_sc was not inhibited by glibenclamide. Dexamethasone (100 nM; 24 hr) not only up-regulated the transcript expression of -ENaC (~4 fold); ₂ (~2 fold) & ₃ (~8 fold) Na⁺,K⁺-ATPase; Kir2.1 (~5 fold), Kir2.2 (~9 fold), Kir2.4 (~3 fold), Kir3.1 (~ 3 fold), Kir3.3 (~2 fold), Kir4.2 (~3 fold ) & Kir7.1 (~2 fold); Sgk1 (~4 fold) and Nedd4-2 (~2 fold), but also down-regulated GR (~3 fold) and 11-HSD1 (~2 fold). Expression of GR and 11-HSD1 was higher than MR and 11-HSD2 in the absence of dexamethasone. Dexamethasone altered transcript expression levels (-ENaC & Sgk1) by activation of the GR but not MR. Proteins were present for , & subunits of ENaC and Sgk1 and expression of - and -ENaC was up-regulated by dexamethasone. These findings are consistent with the genomic stimulation by glucocorticoids of Na⁺ absorption by SCCD and provide an understanding of the therapeutic action of glucocorticoids in the treatment of Meniere's disease.