Role of nitric oxide released from iNANC neurons in airway responsiveness in cats

The precise role of inhibitory nonadrenergic noncholinergic (iNANC) neurons and nitric oxide in airway hyperresponsiveness remains uncertain, The role of NO in the regulation of airway responsiveness was studied in anaestheti zed and mechanically ventilated cats. To assess airway responsiveness, the changes in total pulmonary resistance (R-L) produced by delivering serotonin aerosol to the airways were measured before and after N-omega-nitro-L-arginine methyl ester (L-NAME), or a gang lionic blocker, hexamethonium, which has been reported to block iNANC. Sero tonin was chosen because it causes bronchoconstriction in part by neural re flex. To further clarify the mechanism(s) involved, the effect of inhaled c apsaicin was also determined in animals with sustained bronchoconstriction induced by serotonin after treatment with atropine and propranolol, Inhibition of NO synthase by L-NAME or blockade of iNANC neurons by hexamet honium significantly increased airway responsiveness, However, addition of L-NAME did not further increase airway responsiveness in animals treated wi th hexamethonium. In the presence of atropine and propranolol, inhaled caps aicin caused a marked bronchodilation during serotonin-induced sustained br onchoconstriction. The bronchodilation induced by capsaicin was significant ly suppressed by hexamethonium and by L-NAME, These results suggest that the nitric oxide released from inhibitory nonadr energic noncholinergic neurons is important in modulating the airway respon siveness of cats in vivo.