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.
Yokotani
K
K
Department of Pharmacology, Kochi Medical School, Japan.
Okuma
Y
Y
Osumi
Y
Y
D000315:Adrenalectomy; D000818:Animals; D002395:Catecholamines / Q000097:blood; D002490:Central Nervous System / Q000187:drug effects; D004558:Electric Stimulation; D005744:Gastric Acid / Q000378:metabolism*; D006892:Hydroxydopamines / Q000494:pharmacology; D007276:Injections, Intraventricular; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D014630:Vagus Nerve / Q000502:physiology*
D002395:Catecholamines; D006892:Hydroxydopamines; D009538:Nicotine