Central Inhibition of Gastric Motility by Intravenously Administered Nicotine in Rats

Effects of intravenously (i.v.) administered nicotine on gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. I.v. administered nicotine at 75-300 nmole/kg dose-dependently decreased gastric motility. Decrease in gastric motility induced...

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Bibliographic Details
Published in:Japanese Journal of Pharmacology 1990, Vol.52(3), pp.397-403
Main Authors: NAGATA, Mitsuhiro, OSUMI, Yoshitsugu
Format: Article
Language:English
Subjects:
Anesthesia
Animals
Biological and medical sciences
Brain Stem - physiology
Cholinergic system
Cisterna Magna
Gastrointestinal Motility - drug effects
Hexamethonium Compounds - pharmacology
Injections
Injections, Intravenous
Male
Medical sciences
Neuropharmacology
Neurotransmitters. Neurotransmission. Receptors
Nicotine - administration & dosage
Nicotine - pharmacology
Pharmacology. Drug treatments
Phentolamine - pharmacology
Rats
Rats, Inbred Strains
Vagotomy
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Summary:Effects of intravenously (i.v.) administered nicotine on gastric motility were investigated in urethane-anesthetized rats in which an intragastric balloon had been placed. I.v. administered nicotine at 75-300 nmole/kg dose-dependently decreased gastric motility. Decrease in gastric motility induced by nicotine at the dose of 300 nmole/kg was inhibited by intracisternally administered hexamethonium. Gastric motility was also decreased by intracisternally applied nicotine (1-10 nmole). These doses were much smaller than those by the intracerebroventricular route in our previous report. Bilateral vagotomy significantly suppressed basal gastric motility. In bilaterally vagotomized animals, nicotine at 1 μmole/kg but not 300 nmole/kg given i.v. significantly decreased the gastric motility maintained at a normal level by electrical stimulation of the vagus nerve. This nicotine-induced decrease in gastric motility, under conditions of electrical stimulation of the vagus nerve, was inhibited by pretreatment with phentolamine. These results suggest that a smaller dose of nicotine given i.v. activates nicotiric receptors in the brainstem and elicits vagally-mediated inhibition of gastric motility. Activation of peripheral α-adrenergic mechanisms together with that of central nicotinic mechanisms may be involved in the decreasing effects of a larger dose of nicotine on gastric motility.
ISSN:0021-5198
1347-3506
DOI:10.1254/jjp.52.397