Effects of nedocromil sodium on airway neurogenic mechanisms

Evidence shows that nedocromil sodium has a major inhibitory effect on sensory nerve activation. Animal models in which inhibitory effects have been demonstrated include bradykinin- or ovalbumin-induced plasma extravasation; cigarette smoke- or sulfur dioxide-induced bronchial hyperresponsiveness and increase in inflammatory cells in the airway; and bradykinin-induced airway vasodilatation and nasal mucosal edema. Nedocromil sodium has prevented the edema in human skin induced by substance P and neurokinin A, and, in the isolated rabbit trachea, has prevented substance P-induced potentiation of cholinergic neural responses at preganglionic (but not postganglionic) sites. In vitro, the drug also has inhibited nonadrenergic noncholinergic bronchoconstriction in guinea pig bronchi. Although a protective effect against citric acid-induced cough in the dog has been reported, no data are available from models of enhanced cough reflex, such as that in asthma. Inhibition of sensory nerve activation and prevention of tachykinin release by nedocromil sodium probably contribute to its beneficial effects in the treatment of asthma.