The action of beta-receptors on microvascular endothelium or: is airways plasma exudation inhibited by beta-agonists?

The connections between airway inflammation, plasma exudation and a possible anti-exudative action of beta-agonists are discussed. Asthma involves a response to inflammatory mediators which results in increased microvascular leakage with exudation of plasma into the airways. This plasma exudation is a specific inflammatory response and also a general response in the sense that it is independent of the mechanism sustaining the inflammation. Thus, mucosal exudation of plasma may reflect the subepithelial airway inflammatory process, irrespective of its genesis. In addition, the exudate itself contains many substances which may themselves promote inflammation and be major factors in producing and sustaining acute and chronic airway inflammation. This suggests that drug therapies should be aimed at reducing plasma exudation. Studies in guinea pigs have shown that a number of drugs such as xanthines, cromoglycates, glucocorticoids and beta-agonists may inhibit this exudation, but the effect seems to be attenuated in human mucosal tissue. beta-Agonists appear promising in this respect, but if an anti-exudative effect is confirmed for them, it will be necessary to determine whether this is a direct effect or secondary to their effects on cellular inflammatory processes in the airways.