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2000 Fiscal Year Final Research Report Summary

Effects of nitric oxide on pain perception by primary afferent neurons in inflammation

Research Project

Project/Area Number 11671840
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Functional basic dentistry
Research InstitutionSetsunan University (2000)
Osaka University (1999)

Principal Investigator

MAEDA Sadaaki  Setsunan Univ., Faculty of Pharmaceut.Sci., Professor, 薬学部, 教授 (00135732)

Co-Investigator(Kenkyū-buntansha) SAEKI Makio  Osaka Univ., Faculty of Dentistry, Research associate, 歯学部, 助手 (30273692)
YOSHIOKA Yasuhiro  Setsunan Univ., Faculty of Pharmaceut.Sci., Research associate, 薬学部, 助手 (40330360)
MATSUDA Toshio  Osaka Univ., Faculty of Pharmaceut.Sci., Professor, 薬学部, 教授 (00107103)
Project Period (FY) 1999 – 2000
Keywordsimflammation / cultured trigeminal ganglion cell / nitric oxide / bradykinin / pain / intracellular calcium / writhing reaction
Research Abstract

In primary cultured trigeminal ganglion cells, NOC12, a nitric oxide (NO) donor, potentiated bradykinin (BK)-induced increase in intracellular free calcium concentration ([Ca^<2+>]i). The effect of NOC12 was blocked by carboxy-PTIO (specific NO radical scavenger) and ODQ (guanylate cyclase inhibitor), but not super oxide dismutase. 8-Bromo-cGMP potentiated the rise of [Ca^<2+>]i induced by BK.Both NOC12 and 8-bromo-cGMP did not affect the increase in [Ca^<2+>]i by histamine and carbachol. These results indicate that NO potentiates BK-induced increase in [Ca^<2+>]i by the activation of guanylate cyclase. This also suggests that NO may affect BK-mediated nociceptive responses.
We investigated the effect of NO on kaolin-induced writhing behavior mediated by BK receptors. Intraperitoneal administration of lipopolysaccharide (LPS) in mice increase kaolin-induced writhing reaction, which was inhibited by BK-B2 receptor agonist Hoe140. The increase was inhibited by 2-iminopiperidine, an inducible NO synthase inhibitor. LPS-activated macrophages produced NO in a dose- and time-dependent manner. Pretreatment with 2-iminopiperidine caused a reduction in LPS-stimulated production of NO by peritoneal macrophages. These results indicate that LPS potentiated kaolin-induced writhing through producing NO.
These results suggest that nitric oxide may potentiate pain perception in inflammation.

  • Research Products

    (2 results)

All Other

All Publications (2 results)

  • [Publications] 山田隆史: "一次知覚神経終末における痛みの受容に対する一酸化窒素の作用"大阪大学歯学雑誌. 44巻1号. 1-12 (1999)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yamada, T.: "Effects of nitric oxide on pain perception at primary afferent neurons"Journal of Osaka University Dental School (Japanese). 44(1). 1-13 (1999)

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 2002-03-26  

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