Both avian corticosteroid hormones, aldosterone and corticosterone, increased short-circuit current across the wall of the ceca of the domestic fowl (Gallus domesticus) in vitro. About 80% of this short-circuit current was inhibited by the Na-channel blocking drug amiloride. Corticosterone was about ten times less potent than aldosterone in increasing short-circuit current and it exerted a similar maximal effect. Cortisol (an endogenous corticosteroid hormone in mammals but not birds) was about ten times less potent than corticosterone and this difference appeared to reflect the presence of the 17 alpha-OH group in cortisol. Carbenoxolene, which inhibits 11 beta-hydroxysteroid dehydrogenase, increased the effect of corticosterone. This effect is consistent with inhibition of the metabolism of corticosterone to 11-dehydrocorticosterone. The latter was found to be about 100 times less potent than corticosterone. The effects of both aldosterone and corticosterone (also dexamethasone) were abolished by the mineralocorticoid receptor antagonist spironolactone. The results suggest that corticosterone has an effect similar to aldosterone but in vivo its action may be depressed by the activity of 11 beta-hydroxysteroid dehydrogenase. The sensitivity of the cecal preparations to corticosterone indicates that this hormone could contribute to the regulation of transcecal Na transport (absorption) in vivo.