The composition and volume of the alveolar surface fluid affect effective gas exchange in the adult lung. The alveolar fluid clearance is dependent on the transport of Na and Cl, but precise contributions of concerned ion channels in basal conditions and after stimulation are still debated. We present a novel functional model of rat lung slices suitable for whole-cell patch-clamp characterisation. Slices cultured on paper filters retained a majority of living cells for up to 72 hours following sectioning. When patched in whole-cell configuration, type II pneumocytes in situ had a mean capacitance of 11.61.2 pF and a resting membrane voltage of - 4.3  2.8 mV. Replacement of Na⁺ in the bath with NMDG⁺ significantly decreased inward whole-cell currents, however these currents were not amiloride-sensitive. Exposure of slices to 1 M dexamethasone for 1 hour did not have an effect on ion currents. However chronic exposure to dexamethasone during 24-48 hours induced an increase in Na-entry currents, which became partially inhibitable by amiloride. Acute treatment of type II pneumocytes in situ with 100 M cpt-cAMP resulted in fast hyperpolarization of these cells by 15-20 mV arising from activation of inward Cl-currents sensitive to NPPB, a blocker of CFTR. These results indicate that sodium amiloride-sensitive channels (ENaC) are not present in type II pneumocytes from freshly prepared rat lung slices, however they can be induced by chronic glucocorticoid treatment. They also indicate that in in situ conditions acute beta-adrenergic activation stimulates entry of chloride ions into Type II alveolar cells. Funded by ULB, FNRS and Fonds Defay. VS was a recipient of ERS research fellowship (No306).