The liquid in the lumen of postnatal lung is in a homeostatic state: there is a balance between absorption and secretion, this maintains the lining layer at a mean depth of ~0.15μm (1). The instillation of liquid into the postnatal lungs result in a shift of the balance and net absorption of liquid predominates. The absorption is the result of active sodium movement, across the pulmonary epithelium and the movement of water down its osmotic gradient (2). In a series of experiments, to examine the effect of luminal volume on liquid absorption, adult Wistar rats were anaesthetised using a 1:1:2 mixture of midazolam, fentanyl citrate/fluanisone and water (2.7 ml.kg^-1ip). The animals were ventilated with room air and pulmonary artery and left atrium were catheterised. The lungs were perfused with a modified Ringer’s solution containing 3% albumin. A known volume of liquid, containing an impermeant tracer (Blue D) was instilled into the lungs. The volumes of lung liquid (LL) used were: 10, 15 or 30 ml.kg^-1. Blue D concentration was determined from the absorbance of samples of LL at 620nm and this was used to calculate the change in LL volume with time (J_v). J_v during the first 40 minutes of sampling was the same for all volumes of LL used. During the following 40 minutes, J_v increased in the 30 ml.kg^-1 experiments but remained the same for the other 2 volumes (Table 1). The increase did not involve either the epithelial sodium channel (ENaC) or the cyclic nucleotide gated channel (CNG) as blockers of both channels, amiloride (50μM) and l-cis-diltiazem (100μM) respectively, had no effect on the increase in J_v. In contrast, gadolinium chloride (GdCl₃; 10μM) blocked the increase in J_v (Table 1) suggesting the involvement of stretch-activated channels (SAC). We conclude that the permeability of the postnatal rat pulmonary epithelium is unlikely to have been altered by LL volumes up to 30 ml.kg^-1 and that recruitment of SAC is one mechanism of maintaining homeostatic control. Fisher and Margulies (3) have shown that Na⁺– K⁺-ATPase activity increases with cyclic but not tonic stretch of alveolar type 2 cells in culture. We cannot discount this mechanism in the whole lung but as GdCl₃ prevented the increase in J_v seen at 30 ml.kg^-1, it is likely that this effect is mediated by SAC in the epithelium.