We studied the role of nitric oxide and inhibitory non-adrenergic, non-cholinergic (i-NANC) nerves in the regulation of airway responsiveness in anesthetized and mechanically ventilated cats. Vagal stimulation caused marked bronchodilation in the cats with sustained bronchoconstriction in the presence of atropine and propranolol. The bronchodilation evoked by vagal stimulation was completely abolished by hexamethonium (2 mg/kg). L-NG-nitroarginine methyl ester (L-NAME; 8 mg/kg + 2 mg/kg/min) significantly suppressed the relaxation evoked by vagal stimulation; the effect was particularly noticeable soon after the stimulation. Hexamethonium significantly increased airway responsiveness to serotonin: the PC200 decreased from 0.346 mg/ml (GSEM 1.23) without hexamethonium to 0.44 mg/ml (GSEM 1.63) with hexamethonium (p < 0.05). L-NAME shifted the dose-response curve to serotonin significantly to the left: the PC200 decreased from 0.261 mg/ml (GSEM 1.,40) without L-NAME to 0.056mg/dl (GSEM 1.38) with L-NAME (p < 0.05). Inhalation of citric acid (20%) caused marked bronchodilation during serotonin-induced bronchoconstriction. This bronchodilation occurred in the presence of atropine and propranolol and was inhibited by hexamethonium, therefore it was probably caused by a reflex mediated by i-NANC nerves. Furthermore, the bronchodilation induced by i-NANC nerves was significantly suppressed by L-NAME. These results suggest that nitric oxide is an important i-NANC transmitter that can modulate airway responsiveness.
|ジャーナル||Nihon Kyōbu Shikkan Gakkai zasshi|
|出版ステータス||出版済み - 12月 1995|
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