Microvascular leakage and neurogenic mechanisms may be important components of the inflammatory response in asthmatic airways. We have examined the effects of nedocromil sodium on these responses. In guinea-pig airway, microvascular leakage induced by allergen was significantly inhibited by prior treatment with nedocromil sodium (100 micrograms/kg IV), but this had no effect on histamine-induced leakage and reduced PAF-induced leakage only at a dosage of 5 mg/kg. This suggests that nedocromil sodium acts mainly by preventing the release of inflammatory mediators. Both sulphur dioxide (SO2) and bradykinin cause bronchoconstriction in asthmatic patients, which is likely to be due to a neural mechanism since SO2 activates C-fibre sensory nerve endings in airways. Inhaled nedocromil sodium is effective in inhibiting both SO2- and bradykinin-induced bronchoconstriction, and furthermore reduces the sensation of dyspnoea, indicating a possible action on sensory nerve endings in airways.