Adrenaline was infused intravenously at rates of 0.1-1.0 microgram/min into chronically catheterized fetal lambs (125-141 days gestation) to induce slowing of secretion or reabsorption of lung liquid. There was an electrical potential difference (p.d.) of -0.3 to -9.5 mV (mean -3.4 mV) between lung liquid and plasma (lung liquid negative) during control lung liquid secretion. In response to adrenaline infusion, the p.d. increased (lung lumen more negative) and this change was greatest (1.8 +/- 0.3 mV) in experiments in which reabsorption occurred. Measurements were made of bidirectional fluxes of Na+ and Cl- across the pulmonary epithelium during control lung liquid secretion and during adrenaline infusion. Adrenaline-induced reabsorption of lung liquid was associated with an increase in Na+ flux from lung lumen to plasma. Similar but smaller changes occurred when the adrenaline response was slowing of secretion. The difference between measured flux ratios and those predicted from the forces determining passive flux provided evidence for active transport of Cl- from plasma to lung lumen, as previously demonstrated by Olver & Strang (1974). When adrenaline was infused, there was evidence of active Na+ transport in the direction lung lumen to plasma and an associated decrease in active Cl- transport in the opposite direction. These changes were greatest when the response to adrenaline was reabsorption. Amiloride, when mixed into the lung liquid to give a calculated concentration of 10(-4) M, abolished the changes in p.d. and ion flux induced by adrenaline. In experiments using amiloride concentrations between 10(-8) and 10(-4) M it was shown that 50% inhibition of the reabsorptive response to adrenaline (KI) was induced by 4 X 10(-6) M-amiloride in the lung lumen. Thus adrenaline-induced slowing of secretion or reabsorption of lung liquid is mediated by active Na+ transport from lung lumen to plasma and depends on amiloride-inhibitable Na+ channels on the luminal surface of the pulmonary epithelium.