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    • Modulation of Capsaicin-Evoked Visceral Pain and Referred Hyperalgesia by Protease-Activated Receptors 1 and 2

    DOI Web Site PubMed 被引用文献7件 参考文献49件 オープンアクセス
    • Kawao Naoyuki
      Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University
    • Ikeda Hisao
      Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University
    • Kitano Tomoko
      Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University
    • Kuroda Ryotaro
      Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University
    • Sekiguchi Fumiko
      Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University
    • Kataoka Kazuo
      Department of Neurosurgery, School of Medicine, Kinki University
    • Kamanaka Yoshihisa
      Minase Research Institute, Ono Pharmaceutical Co., Ltd.
    • Kawabata Atsufumi
      Division of Physiology and Pathophysiology, School of Pharmaceutical Sciences, Kinki University

    書誌事項

    公開日
    2004
    資源種別
    journal article
    DOI
    • 10.1254/jphs.94.277
    公開者
    公益社団法人 日本薬理学会

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    説明

    Protease-activated receptors (PARs) 1 and 2 are expressed in capsaicin-sensitive sensory neurons, being anti- and pro-nociceptive, respectively. Given the possible cross talk between PAR-2 and capsaicin receptors, we investigated if PAR-2 activation could facilitate capsaicin-evoked visceral pain and referred hyperalgesia in the mouse and also examined the effect of PAR-1 activation in this model. Intracolonic (i.col.) administration of capsaicin triggered visceral pain-related nociceptive behavior, followed by referred hyperalgesia. The capsaicin-evoked visceral nociception was suppressed by intraperitoneal (i.p.) TFLLR-NH2, a PAR-1-activating peptide, but not FTLLR-NH2, a control peptide, and unaffected by i.col. TFLLR-NH2. SLIGRL-NH2, a PAR-2-activating peptide, but not LRGILS-NH2, a control peptide, administered i.col., facilitated the capsaicin-evoked visceral nociception 6 – 18 h after administration, while i.p. SLIGRL-NH2 had no effect. The capsaicin-evoked referred hyperalgesia was augmented by i.col. SLIGRL-NH2, but not LRGILS-NH2, 6 – 18 h after administration, and unaffected by i.p. SLIGRL-NH2, and i.p. or i.col. TFLLR-NH2. Our data suggest that PAR-1 is antinociceptive in processing of visceral pain, whereas PAR-2 expressed in the colonic luminal surface, upon activation, produces delayed sensitization of capsaicin receptors, resulting in facilitation of visceral pain and referred hyperalgesia.<br>

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