Abstract
Monkey (crab-eating monkey) was used as an experimental animal in this study since the pharmacological properties of isolated monkey bronchial smooth muscle were reported to be qualitatively similar to human muscle. Nicotine (10(-5)-10(-3) M) induced a phasic contraction in the isolated monkey bronchial smooth muscle preparation. The contractile response to nicotine was abolished by hexamethonium and atropine and potentiated by physostigmine but not influenced by tetrodotoxin. These results suggest that the response to nicotine was mediated through the release of acetylcholine, and that the nicotine-induced response may be produced through a sodium action potential independent process. In addition, the mechanisms of action of nicotine on the bronchial preparation of crab-eating monkey were similar to those of nicotine on the rabbit bronchial preparation but not to those on the isolated guinea-pig bronchus.
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