Dexamethasone (DEX) stimulates alveolar reabsorption by stimulating the expression of ENaC and Na/K‐ATPase. Nasal potentials (NP) have been used repeatedly to estimate changes in alveolar reabsorption. However, in a clinical trial on DEX‐treatment (Maggiorini AIM 2006) we found no effect of DEX on NP. Therefore we tested whether a similar DEX‐treatment of rats affects both NP and the expression of Na‐transporters in nasal epithelium, trachea, primary alveolar epithelial cells (AII), and in leukocytes. Rats were treated with DEX (2mg/kg/day; i.p.) for up to three days. NP was measured after anesthesia, and tissues were removed for mRNA preparation. In a separate series of experiments lung reabsorption was measured after fluid instillation. Total NP was increased (+2mV) after 48hDEX but the amiloride‐sensitive component was not affected. DEX did not affect. α,β,γ‐ENaC in nasal epithelium and leukocytes but increased it in trachea and AII cells (50–100%). DEX did not affect α1,β1‐Na/K‐ATPase mRNA in nasal epithelium but increased α1 mRNA in trachea (100%). Leukocyte α1 mRNA was decreased by 50%. CFTR, nedd‐4 and sgk‐1 mRNAs were not affected. DEX stimulated alveolar fluid reabsorption by increasing its amiloride‐sensitive component. These results indicate that a) NP do not reflect alveolar ion transport activity upon treatment with DEX, and that b) DEX stimulation of Na‐transport varies across lung epithelia.