Bradykinin-12-lipoxygenase-VR1 signaling pathway for inflammatory hyperalgesia.

نویسندگان

  • Jieun Shin
  • Hawon Cho
  • Sun Wook Hwang
  • Jooyoung Jung
  • Chan Young Shin
  • Soon-Youl Lee
  • So Hee Kim
  • Myung Gull Lee
  • Young Hae Choi
  • Jinwoong Kim
  • Nicole Alessandri Haber
  • David B Reichling
  • Sachia Khasar
  • Jon D Levine
  • Uhtaek Oh
چکیده

The capsaicin-sensitive vanilloid receptor (VR1) was recently shown to play an important role in inflammatory pain (hyperalgesia), but the underlying mechanism is unknown. We hypothesized that pain-producing inflammatory mediators activate capsaicin receptors by inducing the production of fatty acid agonists of VR1. This study demonstrates that bradykinin, acting at B2 bradykinin receptors, excites sensory nerve endings by activating capsaicin receptors via production of 12-lipoxygenase metabolites of arachidonic acid. This finding identifies a mechanism that might be targeted in the development of new therapeutic strategies for the treatment of inflammatory pain.

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عنوان ژورنال:
  • Proceedings of the National Academy of Sciences of the United States of America

دوره 99 15  شماره 

صفحات  -

تاریخ انتشار 2002