Sodium and anion transport across the avian uterine (shell gland) epithelium

The uterine (shell gland) epithelium from the domestic chicken was mounted in Ussing chambers, bathed in symmetric avian saline solution on both apical and basolateral aspects and voltage clamped at 0 mV. The epithelium exhibited a basal short circuit current (I_sc) that was partially inhibited by the epithelial Na⁺ channel (ENaC) blockers, amiloride and benzamil (IC₅₀ values of 0.8 and 0.12 μmol l^-1, respectively). Inhibition of basal Na⁺ absorption by 10 μmol l^-1 amiloride was confirmed by measurements of transepithelial Na⁺ and Cl^- fluxes, where inhibition of the apical-to-basolateral and net Na⁺ flux occurred, but no significant effects on Cl^- fluxes were detected. The amiloride-insensitive portion of the basal I _sc was both Cl^- and HCO₃^- dependent and was inhibited by the Cl^- channel blocker, diphenyl-2-carboxylate (DPC; 100 μmol l^-1). Stimulation with 8-(4-chlorophenylthio)- cyclic 3′-5′, adenosine monophosphate (8-cpt cAMP) produced a sustained increase in I_sc that was dependent on both Cl^- and HCO₃^-. The magnitude of the amiloride-sensitive I _sc was approximately twofold greater in birds where shell formation was complete, but oviposition had not yet occurred. In addition, the amiloride-sensitive I_sc was greater in hens over the age of 55 weeks and in molting birds. The anion-dependent component of the basal I_sc was reduced in older birds, and electrogenic HCO₃^- transport was nearly absent in molting birds. These results demonstrated that electrogenic Na⁺ transport in avian shell gland was similar to the mammalian uterine epithelium and increased with age and during molting. Electrogenic Cl^- and HCO₃^- transport were coupled under basal and cAMP stimulated conditions and basal anion transport decreased with age and during molting.