Alveolar fluid transport is driven by active Na⁺ transport but the ion channels underlying this important process are not well understood. Early studies of other absorptive tissues established that apical Na⁺ entry occurred via highly selective epithelial Na⁺ channels (ENaC) but most early studies failed to identify such channels in distal lung epithelia. It was therefore suggested that Na⁺ entry in these cells might occur via non-selective cation channels. However, our studies of fetal distal lung epithelial (FDLE) cells identified a highly selective apical Na⁺ conductance (G_Na) that could be acutely regulated via b-adrenoceptors. Interestingly, this acute control over G_Na was dependent upon thyroid and glucocorticoid hormones; this is consistent with data from studies of fetal lambs, which show that these three hormones are all needed for lung liquid clearance. More recent electrophysiological studies of single H441 cells have identified a glucocorticoid-induced Na⁺ conductance identical with that associated with ENaC expression in other absorptive tissues. The magnitude of this conductance is low,allowing only ~27 pA cell^-1 of inward Na⁺ in resting cells but our analyses indicate this modest conductance can account for the spontaneous I_SC generated by polarised cells. Our data thus suggest that highly selective Na⁺ channels underlie lung Na⁺ transport.