Nicotine stimulates esophageal peristaltic contractions in cats by a central mechanism

The aim of the present study was to 1) characterize nicotine-induced peristalsis in the feline esophagus and 2) determine the site of action of nicotine. Experiments were done on ketamine-sedated cats. Esophageal contractions were measured using a multilumen catheter assembly system. After recording 1 degree and 2 degrees peristaltic sequences nicotine (50-100 micrograms/kg iv) was administered. Nicotine induced a peristaltic contraction through the esophageal striated and smooth muscle part of the esophagus, which was not associated with any mylohyoid electromyogram activity or pharyngeal response, although the upper esophageal sphincter did relax. Addition of either atropine (20-50 micrograms/kg iv) or hexamethonium (10-20 mg/kg iv), a peripherally acting nicotinic antagonist, did not affect the striated muscle portion of the nicotine-induced esophageal contractile response but antagonized the smooth muscle response. However, mecamylamine (0.5-1 mg/kg iv), a ganglionic antagonist that crosses the blood-brain barrier, abolished the esophageal response to nicotine. Succinylcholine (0.5-1 mg/kg iv) abolished the striated muscle response without affecting the nicotine-induced smooth muscle contractility. Finally, the nicotine-induced peristaltic sequence was abolished after bilateral cervical vagotomy. In conclusion, nicotine, administered peripherally, activates central brain stem mechanisms that mediate a peristaltic sequence through the feline esophagus.