Tetrodotoxin-resistant response to nicotine in rabbit bronchial preparation.
The mode of action of nicotine was studied in a rabbit bronchial preparation. Nicotine (3 X 10(-5)-10(-3) M) produced a phasic contraction. No inhibitory response to nicotine was observed. The contractile response to nicotine was inhibited by hexamethonium, pentolinium and atropine but not by tetrodotoxin. Nicotine increased the efflux of tritium from preparations which had been labelled with [3H]choline. Tetrodotoxin did not inhibit the nicotine-evoked tritium release from the bronchial preparation. The results indicate that the release of acetylcholine evoked by nicotine was not influenced by tetrodotoxin in this preparation, and that the nicotine-induced response may be produced mainly through a sodium action potential-independent process. We could not rule out a contribution by acetylcholine released from the acetylcholine store in the smooth muscle in the contractile mechanisms for nicotine.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001980:Bronchi / Q000187:drug effects* / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004351:Drug Resistance; D004558:Electric Stimulation; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009538:Nicotine / Q000494:pharmacology*; D011817:Rabbits; D013779:Tetrodotoxin / Q000494:pharmacology*
D013779:Tetrodotoxin; D009538:Nicotine; D000109:Acetylcholine