It is clear that the central airway epithelium plays an important role in restricting access of inhaled solutes to sub-epithelial airway wall structures. Non-specific airway hyperreactivity to spasmogens in asthma may result partly as a consequence of the compromise of the epithelium as a barrier to solute diffusion. However, impaired epithelial production and release of smooth muscle relaxant factor(s) may also contribute to airway hyperresponsiveness. Virally precipitated asthma also involves inflammation-induced epithelial damage. Beta-adrenoceptor hypofunction induced by respiratory viruses may also contribute to bronchial obstruction.