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Vol. 83, Issue 5, 1432-1437, 1997
Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka 812, Japan
Received 17 March 1997; accepted in final form 15 July 1997.
Matsumoto, Koichiro, Hisamichi Aizawa, Shohei Takata,
Hiromasa Inoue, Naotsugu Takahashi, and Nobuyuki Hara.
Nitric oxide derived from sympathetic nerves regulates airway
responsiveness to histamine in guinea pigs. J. Appl.
Physiol. 83(5): 1432-1437, 1997.
Nitric oxide
(NO), which can be derived from the nervous system or the epithelium of
the airway, may modulate airway responsiveness. We investigated how NO
derived from the airway nervous system would affect the airway
responsiveness to histamine and acetylcholine in mechanically
ventilated guinea pigs. An NO synthase inhibitor NG-nitro-L-arginine
methyl ester (L-NAME) (1 mmol/kg
ip) significantly enhanced airway responsiveness to histamine but not
to acetylcholine. Its enantiomer
D-NAME (1 mmol/kg ip), in
contrast, had no effect. The
L-NAME-induced airway
hyperresponsiveness was still observed in animals pretreated with
propranolol (1 mg/kg iv) and atropine (1 mg/kg iv). Pretreatment with
the ganglionic blocker hexamethonium (2 mg/kg iv) completely abolished
enhancing effect of L-NAME on airway responsiveness. Bilateral cervical vagotomy did not alter the
L-NAME-induced airway
hyperresponsiveness, whereas sympathetic stellatectomy completely
abolished it. Results suggest that NO that was presumably derived from
the sympathetic nervous system regulates airway responsiveness to
histamine in guinea pigs.
vagal nerve; stellate ganglia
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