Microvascular leakage, an essential component of inflammation, probably plays a critical role in asthma in producing plasma exudation and thickening of the bronchial mucosa which may underlie airway hyperresponsiveness. Several therapeutic approaches are possible to reduce this leakage, by blocking either the effects or the release of inflammatory mediators which induce the leakage. Drugs with these actions might be too specific to be of therapeutic value if many mediators are involved, as seems increasingly likely. Reduction of blood flow using selective vasoconstrictors is a more attractive approach and alpha 1-adrenoceptor agonists may be of value. Drugs that act directly on endothelial cells are probably the most useful, since they would be effective irrespective of the mechanism of leakage. Corticosteroids probably have this property, but whether beta-agonists or theophylline are clinically effective against airway microvascular leakage is not yet certain. The development of new drugs which can inhibit microvascular leakage is an important therapeutic approach for the future.