There is increasing evidence that the sensory nerves of the airway play a role in the asthmatic response. Nerve endings are exposed by the epithelial shedding that occurs with asthma. They may become sensitized and activated by inflammatory mediators and may release neuropeptides that then spread and amplify the inflammatory process in the airways. Nedocromil sodium may prevent the sensory nerves from becoming sensitized and inhibit their activation. This possibility is suggested because nedocromil is highly effective against several indirect challenges that involve sensory nerve stimulation. Nedocromil sodium was able to inhibit the bronchoconstriction induced in patients with asthma by exposure to bradykinin, sulfur dioxide, metabisulfite, and ultrasonically nebulized water. Cough, which is a prominent symptom of asthma, is believed to be a result of sensory nerve activation. In several long-term clinical studies, nedocromil sodium reduces the severity of cough among patients with asthma. Studies are needed to define how nedocromil sodium acts on the sensory nerves.