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Perivascular Sympathetic Nerve-Mediated Vasodilation in The Rat Mesenteric Resistance Artery

Research Project

Project/Area Number 13672389
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field 応用薬理学・医療系薬学
Research InstitutionOKAYAMA UNIVERSITY

Principal Investigator

KAWASAKI Hiromu  Okayama University Graduate School of Natural Science and Technology, Professor, 大学院・自然科学研究科, 教授 (60125151)

Co-Investigator(Kenkyū-buntansha) KUROSAKI Yuuji  Okayama University Faculty of Pharmacuitical Sciences Professor, 薬学部, 教授 (90161786)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥2,300,000 (Direct Cost: ¥2,300,000)
KeywordsSympathetic adrenergic nerves / Calcitonin gene-related peptide (CGRP)-nerves / Nicotine / Vanilloid receptors / Adrenergic neurotransmitters / Proton / Rat mesenteric resistance artery / 神経伝達物質
Research Abstract

Nicotine has been shown to, in the rat mesenteric artery, cause a concentration-dependent and endothelium-independent vasodilator response, which is mediated by capsaicin-sensitive nerves and is associated with the intact adrenergic nerves. In the present study, mechanisms underlying the nicotine-induced vasodilation where further investigated in mesenteric resistance blood vessels of the Wistar rat. Isolated mesenteric vascular beds without endothelium were perfused with Krebs solution and contracted by 2-5 μM methoxamine and perfusion pressure was measured with a pressure transducer.
Perfusion of nicotine (1 to 100 μM) for 1 min caused a concentration-dependent vasodilation. The nicotine-induced vasodilation was inhibited by the vanilloid receptor antagonists, capsazepine(1 to 10 μM) and ruthenium red (1 to 30 μM), but did not by DOPA receptor antagonist (L-DOPA CHE), dopamine D1 and D2 receptor antagonist (SCH 23390 and haloperidol), ATP P2X receptor desensitizing agent (α, β-methylene ATP), neuropeptide Y1 receptor antagonist (BIBP3226), and adenosine A2 receptor antagonist (8-SPT). Catecholamine metabolites including normetanephrine and 3-methoxytyramine but not homovanillic acid induced concentration dependent-vasodilation, which was not inhibited by capsaicin treatment. The proton pump inhibitor, omeprazol, inhibited the nicotine-induced vasodilation in a concentration-dependent manner. These results suggest that vanilloid receptors on CGRPergic nerves may be activated by proton released by nicotine to cause vasodilation in the mesenteric resistance artery of the rat.

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (3 results)

All Other

All Publications (3 results)

  • [Publications] H.Shiraki, H.Kawasaki, S.Tezuka, A.Nakatsuma, H.Nawa, H.Araki, Y.Gomita, Y.Kurosaki: "Adrenergic nerves mediate acetylcholine-induced endothelium-independent vasodilation in the rat mesenteric resistance artery"European Journal of Pharmacology. 419. 231-242 (2001)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Hinako Shiraki, Hiromu Kawasaki, Satoko Tezuka, Akira Nakatsuma, Hideki Nawa, Hiroaki Araki, Yutaka Gomita, Yuji Kurosaki: "Adrenergic nerves mediate acetylcholine-induced endothelium-independent vasodilation in the rat mesenteric resistance artery"European Journal of Pharmacology. 419. 231-242 (2001)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Shiraki H., Kawasaki H., Tezuka S., Nakatuma A., Nawa H., Araki H., Gomita Y., Kurosaki Y.: "Adrenergic nerves mediate acetylcholine-induced endothelium-independent vasodilation in the rat mesenteric resistance artery"European Journal of Pharmacology. 419. 231-242 (2001)

    • Related Report
      2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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