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

Yokotani, Kunihiko; Okuma, Yasunobu; Osumi, Yoshitsugu

doi:10.1254/jjp.45.288

Cited by 2 publications

(3 citation statements)

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“…Central administration of nicotine increases plasma levels of norepinephrine and epinephrine (21, 22) and induces norepinephrine release in the CNS (29, 30). Thus, we tested whether central or peripheral norepinephrine is involved in the central nicotine‐induced peripheral IL‐6 responses.…”

Section: Resultsmentioning

confidence: 99%

“…The marked inhibition of central nicotine‐induced plasma IL‐6 levels by chemical sympathectomy suggests that the peripheral sympathetic nervous system is crucially involved in the phenomenon. Central administration of nicotine has been shown to stimulate sympathetic outflow, as demonstrated by increased plasma norepinephrine levels (21, 22). The result that centrally administered nicotine, but not the maximally effective doses (105 or 350 ng/mouse) of peripherally administered nicotine, induces an increase in plasma IL‐6 levels strongly suggests that the site of nicotinic receptor modulation of peripheral IL‐6 response resides in the CNS.…”

Section: Discussionmentioning

confidence: 99%

“…For the central nicotine‐induced plasma IL‐6 response, the results of the present study suggest that α 1 ‐, α 2 ‐, and β 2 ‐adrenoreceptors may be involved. The finding suggesting the involvement of β 2 ‐adrenoreceptors implicates epinephrine in the nicotine‐induced plasma IL‐6 response, because norepinephrine is a very weak agonist for β 2 ‐adrenore‐ceptors compared with epinephrine, and plasma levels of epinephrine as well as norepinephrine have been shown to increase after central administration of nicotine (21, 22).…”

Section: Discussionmentioning

confidence: 99%

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Central injection of nicotine increases hepatic and splenic interleukin 6 (IL‐6) mRNA expression and plasma IL‐6 levels in mice: involvement of the peripheral sympathetic nervous system

Song

Jung

et al. 1999

FASEB j.

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Accumulating evidence suggests that plasma levels of interleukin 6 (IL-6), a major cytokine stimulating the synthesis of acute-phase proteins, are intimately regulated by the central nervous system. Nicotine, one of the major drugs abused by humans, has been shown to affect immunological functions. In the present study, effects of intracerebroventricular (i.c.v.) injection of nicotine on plasma IL-6 levels were investigated in mice. Nicotine administered i.c.v. dose-dependently increased plasma IL-6 levels; the lowest effective dose was 0.3 ng/mouse and the maximal effect was attained with the dose of 105 ng/mouse. The nicotine (105 ng/mouse, i.c.v.)-induced plasma IL-6 levels peaked at 3 h and approached basal levels 6 h after injection. Mecamylamine, a nicotinic receptor antagonist, blocked nicotine-induced plasma IL-6 levels. Depletion of peripheral norepinephrine with 6-hydroxydopamine [100 mg/kg, intraperitoneal (i. p.)] inhibited the nicotine-induced plasma IL-6 levels by 57%, whereas central norepinephrine depletion with 6-hydroxydopamine (50 microgram/mouse, i.c.v.) had no effect. Pretreatment with prazosin (alpha1-adrenergic antagonist; 1 mg/kg, i.p.), yohimbine (alpha2-adrenergic antagonist; 1 mg/kg, i.p.), and ICI-118,551 (beta2-adrenergic antagonist; 2 mg/kg, i.p.), but not with betaxolol (beta1-adrenergic antagonist; 2 mg/kg, i.p.), inhibited nicotine-induced plasma IL-6 levels. Among the peripheral organs, including the pituitary, adrenals, heart, lung, liver, spleen, and lymph nodes, nicotine (105 ng/mouse, i.c.v.) increased IL-6 mRNA expression only in the liver and spleen, which was inhibited by peripheral norepinephrine depletion. These results suggest that stimulation of central nicotinic receptors induces plasma IL-6 levels and IL-6 mRNA expression in the liver and spleen via the peripheral sympathetic nervous system, alpha1-, alpha2-, and beta2-adrenoreceptors being involved.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%