New evidence indicates that alveolar fluid clearance is driven by active sodium transport across the alveolar epithelium. Several in vivo as well as some in vitro studies indicate that vectorial sodium transport drives fluid clearance across the alveolar epithelium. This transport process can be upregulated by both catecholamine-dependent and catecholamine-independent mechanisms. Water transport appears to move across the alveolar epithelium primarily via transcellular water channels, recently termed aquaporins. Under some conditions, net alveolar fluid clearance continues even in the presence of acute lung injury. It is now possible to study the rate and mechanisms of alveolar fluid clearance in patients with either hydrostatic or increased permeability pulmonary edema. In addition, it may be possible to increase the rate of alveolar fluid clearance and hence the resolution of pulmonary edema in some patients, using aerosolized beta-adrenergic agonist therapy.