• Y Takahashi, H Ohno, and M Misawa.
• Department of Pharmacology, SS Pharmaceutical Co., Ltd., Narita, Japan.
• Eur. J. Pharmacol. 1996 Apr 29; 302 (1-3): 89-97.

AbstractThe reflex tracheal response induced by bronchoconstriction was investigated using a newly devised tracheo-bronchi preparation in anesthetized guinea pigs. Tracheal constriction and subsequent dilatation were observed in response to bronchoconstriction induced by the inhalation of 0.001-0.01% histamine and 0.003-0.03% acetylcholine. These tracheal responses were abolished by cervical vagotomy or treatment of the tracheal site with 1% tetrodotoxin. Tracheal constriction and dilatation were significantly inhibited by 0.1% atropine and 1% propranolol, respectively. When high tracheal tone was induced by 0.01% serotonin, the residual tracheal dilatation observed in the presence of propranolol was enhanced, while dilatation was completely inhibited by 1% hexamethonium. Dilatation was also suppressed by 1% N omega-nitro-L-arginine methyl ester (L-NAME) and 1% methylene blue. The tracheal constriction produced by bronchoconstriction was significantly enhanced by propranolol 2 mg/kg, i.v. and L-NAME 10 mg/kg, i.v. These results demonstrate that a vagally mediated reflex tracheal response (constriction followed by dilatation) is induced by bronchoconstriction in anesthetized guinea pigs. Cholinergic nerves may mediate the constriction, and adrenergic and nonadrenergic noncholinergic (NANC) inhibitory nerves may mediate the dilatation. Furthermore, NO may be involved in the NANC reflex tracheal dilatation.

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