Intracerebroventricularly administered nicotine inhibits vagally stimulated gastric acid output in rats by activating the central sympatho-adrenal outflow.

The effect of intracerebroventricularly (i.c.v.) administered nicotine was investigated in urethane-anesthetized rats. I.c.v., but not intravenously, administered nicotine (300 and 600 nmole/animal) inhibited the increase in gastric acid output induced by electrical stimulation of the vagus nerve. This antisecretory effect of nicotine was abolished by combined pretreatment with adrenalectomy and 6-hydroxydopamine (50 mg/kg, i.v., 3 days before). I.c.v.-administered nicotine also raised the blood levels of catecholamines. These observations suggest that i.c.v. administered nicotine leads to excitation of the central sympatho-adrenomedullary outflow and inhibits gastric acid output induced by stimulation of the vagus nerve.