The precise mechanism or mechanisms whereby cromolyn sodium and nedocromil sodium exert their antiasthmatic activities is unknown. Early work suggested that these agents act by "stabilizing" mast cells, preventing mediator release. However, several other compounds exhibit greater potency for stabilization of mast cells yet possess no clinical efficacy in asthma. This suggests that the therapeutic activity of cromolyn sodium and nedocromil sodium in asthma is related to one or more other pharmacological mechanisms. Postulates include inhibitory effects on irritant receptors, nerves, plasma exudation, and inflammatory cells in general.
Cromolyn sodium and nedocromil sodium attenuate bronchospasm induced by various stimuli, including antigen, exercise, cold dry air, and sulfur dioxide. They suppress inflammatory cell influx and chemotactic activity along with antigen-induced bronchial hyperreac-tivity. Also inhibited is C-fiber sensory nerve activation in animal models, which may in turn suppress reflex-induced bronchospasm.
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