低剂量的京都啡肽（酪氨酸-精氨酸）通过伤害感受器末梢释放P物质诱导伤害性反应。
Low dose of kyotorphin (tyrosine-arginine) induces nociceptive responses through a substance P release from nociceptor endings.
作者信息
Inoue M, Yamada T, Ueda H
机构信息
Department of Molecular Pharmacology and Neuroscience, Nagasaki University School of Pharmaceutical Sciences, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan.
出版信息
Brain Res Mol Brain Res. 1999 Jun 8;69(2):302-5. doi: 10.1016/s0169-328x(99)00133-3.
The intraplantar injection of kyotorphin (Kyo) elicited nociceptive flexor responses in mice in a dose-dependent manner between 0.1 and 100 fmol. These actions were completely blocked by substance P (NK1) receptor antagonists, such as CP-96345 and CP-99994, but not by their inactive derivatives, CP-96344 or CP-100263, nor by MEN-10376, an NK2 antagonist. Kyo-responses were also abolished by the local pretreatment with capsaicin to deplete substance P from nociceptor endings, and in tachykinin 1 gene K/O mice. These findings suggest that Kyo indirectly stimulates nociceptor endings through a local substance P release.
足底注射京都啡肽（Kyo）可在0.1至100飞摩尔之间以剂量依赖的方式引起小鼠伤害性屈肌反应。这些作用可被P物质（NK1）受体拮抗剂如CP - 96345和CP - 99994完全阻断，但不能被其无活性衍生物CP - 96344或CP - 100263阻断，也不能被NK2拮抗剂MEN - 10376阻断。用辣椒素进行局部预处理以耗尽伤害感受器末梢中的P物质，以及在速激肽1基因敲除小鼠中，Kyo反应也被消除。这些发现表明，Kyo通过局部释放P物质间接刺激伤害感受器末梢。
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