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P物质和辣椒素诱导的大鼠膝关节机械性痛觉过敏；缓激肽B1和B2受体的作用

Substance P and capsaicin-induced mechanical hyperalgesia in the rat knee joint; the involvement of bradykinin B1 and B2 receptors.

作者信息

Davis A J, Perkins M N

机构信息

Sandoz Institute for Medical Research, London.

出版信息

Br J Pharmacol. 1996 Aug;118(8):2206-12. doi: 10.1111/j.1476-5381.1996.tb15664.x.

DOI:10.1111/j.1476-5381.1996.tb15664.x
PMID:8864563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1909860/
Abstract
  1. Substance P (SP) and capsaicin induced a mechanical hyperalgesia when injected into rat knee joints. 2. The NK1 receptor antagonists CP 99994 (10-100 nmol) and RP 67580 (0.1-1 nmol) blocked the development of, and also reversed, SP-induced hyperalgesia. Capsaicin (10 nmol)-induced hyperalgesia was blocked by capsazepine (0.5-5 nmol). 3. Capsaicin-induced hyperalgesia was prevented and reversed by the NK1 receptor antagonists CP 99994 (100 nmol) and RP 67580 (1 nmol). 4. The bradykinin B2 receptor antagonist icatibant (5 pmol) blocked the development of both SP and capsaicin-induced hyperalgesia. Icatibant (100 pmol kg-1, i.v.) also reversed an established SP and capsaicin-induced hyperalgesia. 5. Both low dose SP (1 nmol) and capsaicin (1 nmol)-induced hyperalgesia were potentiated by the kininase II inhibitor captopril (100 micrograms). 6. The B1 receptor antagonists desArg9Leu8-bradykinin (BK) (0.5-5 nmol) and desArg10[Hoe 140] (5-50 pmol) only blocked the development of SP-induced hyperalgesia for 30 min after administration. desArg9Leu8-BK (10 nmol kg-1 i.v.) did not reverse an established SP-induced hyperalgesia. 7. Capsaicin-induced hyperalgesia was blocked by desArg9Leu8-BK (0.5 nmol) and this antagonist also reversed an established capsaicin-induced hyperalgesia. 8. Interleukin-1 receptor antagonist (IL-1ra 0.1 microgram) reduced the development of SP-induced hyperalgesia up to 4 h after administration, but did not reverse an established hyperalgesia. IL-1ra (0.1 microgram) also blocked the development of and reversed an established capsaicin-induced hyperalgesia. 9. Indomethacin pretreatment (1 mg kg-1, s.c.) did not reduce the development of either SP- or capsaicin-induced hyperalgesia but following indomethacin-pretreatment desArg9Leu8-BK (10 nmol kg-1, i.v.) failed to reverse a capsaicin-induced hyperalgesia. 10. In conclusion, both SP and capsaicin can induce behavioural hyperalgesia when injected into the knee joint of rats. In addition, blockade of NK1, bradykinin B1, B2 and IL-1 beta receptors can substantially modulate this hyperalgesia.
摘要
  1. P物质（SP）和辣椒素注入大鼠膝关节时可诱发机械性痛觉过敏。2. NK1受体拮抗剂CP 99994（10 - 100纳摩尔）和RP 67580（0.1 - 1纳摩尔）可阻止SP诱发的痛觉过敏的发展，并使其逆转。辣椒素（10纳摩尔）诱发的痛觉过敏可被辣椒素受体拮抗剂（0.5 - 5纳摩尔）阻断。3. NK1受体拮抗剂CP 99994（100纳摩尔）和RP 67580（1纳摩尔）可预防并逆转辣椒素诱发的痛觉过敏。4. 缓激肽B2受体拮抗剂艾替班特（5皮摩尔）可阻止SP和辣椒素诱发的痛觉过敏的发展。艾替班特（100皮摩尔/千克，静脉注射）也可逆转已形成的SP和辣椒素诱发的痛觉过敏。5. 低剂量SP（1纳摩尔）和辣椒素（1纳摩尔）诱发的痛觉过敏可被激肽酶II抑制剂卡托普利（100微克）增强。6. B1受体拮抗剂去精氨酸9亮氨酸8 - 缓激肽（BK）（0.5 - 5纳摩尔）和去精氨酸10[Hoe 140]（5 - 50皮摩尔）仅在给药后30分钟内阻止SP诱发的痛觉过敏的发展。去精氨酸9亮氨酸8 - BK（10纳摩尔/千克，静脉注射）不能逆转已形成的SP诱发的痛觉过敏。7. 去精氨酸9亮氨酸8 - BK（0.5纳摩尔）可阻断辣椒素诱发的痛觉过敏，该拮抗剂也可逆转已形成的辣椒素诱发的痛觉过敏。8. 白细胞介素 - 1受体拮抗剂（IL - 1ra 0.1微克）在给药后长达4小时内可减少SP诱发的痛觉过敏的发展，但不能逆转已形成的痛觉过敏。IL - 1ra（0.1微克）也可阻止并逆转已形成的辣椒素诱发的痛觉过敏。9. 吲哚美辛预处理（1毫克/千克，皮下注射）不能减少SP或辣椒素诱发的痛觉过敏的发展，但在吲哚美辛预处理后，去精氨酸9亮氨酸8 - BK（10纳摩尔/千克，静脉注射）不能逆转辣椒素诱发的痛觉过敏。10. 总之，SP和辣椒素注入大鼠膝关节时均可诱发行为性痛觉过敏。此外，阻断NK1、缓激肽B1、B2和IL - 1β受体可显著调节这种痛觉过敏。

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