Nicotine facilitates reinnervation of phenol-injured perivascular adrenergic nerves in the rat mesenteric resistance artery

Shingo Takatori, Hidetoshi Fujiwara, Kenta Hagimori, Narumi Hashikawa-Hobara, Ayako Yokomizo, Fusako Takayama, Panot Tangsucharit, Nobufumi Ono, Hiromu Kawasaki

Research output: Contribution to journalArticlepeer-review

3 Citations (Scopus)


Nicotine has been shown to have neuroprotective and neurotrophic actions in the central nervous system. To elucidate the peripheral neurotrophic effects of nicotine, we determined whether nicotine affected the reinnervation of mesenteric perivascular nerves following a topical phenol treatment. A topical phenol treatment was applied to the superior mesenteric artery proximal to the abdominal aorta in Wistar rats. We examined the immunohistochemistry of the distal small arteries 7 days after the treatment. The topical phenol treatment markedly reduced the density of tyrosine hydroxylase (TH)-LI and calcitonin gene-related peptide (CGRP)-LI fibers in these arteries. The administration of nicotine at a dose of 3 mg/kg/day (1.5 mg/kg/injection, twice a day), but not once a day or its continuous infusion using a mini-pump significantly increased the density of TH-LI nerves without affecting CGRP-LI nerves. A pretreatment with nicotinic acetylcholine receptor antagonists hexamethonium, mecamylamine, and methyllycaconitine, but not dextrometorphan, canceled the TH-LI nerve reinnervation induced by nicotine. Nicotine significantly increased NGF levels in the superior cervical ganglia (SCG) and mesenteric arteries, but not in the dorsal root ganglia, and also up-regulated the expression of NGF receptors (TrkA) in the SCG, which were canceled by hexamethonium. These results suggested that nicotine exhibited neurotrophic effects that facilitated the reinnervation of adrenergic TH-LI nerves by activating α7 nicotinic acetylcholine receptor and NGF in the SCG.

Original languageEnglish
Pages (from-to)1-9
Number of pages9
JournalEuropean Journal of Pharmacology
Publication statusPublished - Feb 5 2015


  • Chemical compoundsstudiedinthisarticle:
  • Dextrometorphanhydrobromide(PubChem CID: 5464025) Hexamethoniumbromide(PubChemCID: 5938)
  • Mecamylamine hydrochloride(PubChem CID: 13221)
  • Methyllycaconitinecitrate(PubChemCID: 16219626)
  • Nervegrowthfactor
  • Nicotine
  • Nicotine hydrogentartratesalt(PubChem CID: 11957628)
  • Nicotinicacetylcholinereceptor
  • Rat mesentericartery
  • Tyrosine hydroxylase-containingadrenergic nerves
  • α7

ASJC Scopus subject areas

  • Pharmacology


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