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Bradykinin is involved in hyperalgesia induced by Bothrops jararaca venom

机译:缓激肽参与了由Broprops jararaca毒液诱导的痛觉过敏

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Bradykinin is involved in hyperalgesia (pain hypersensitivity) induced by Bothrops jararaca venom-intraplantar injection of B. jararaca venom (5 mug/paw) in rats caused hyperalgesia, which peaked 1 h after venom injection. This phenomenon was not modified by promethazine, (H-1 receptor antagonist), methysergide (5-HT receptor antagonist), guanethidine (sympathetic function inhibitor), anti-TNF-alpha or anti-interleukin-1 antibodies or by the chelating agent CaNa(2)EDTA. Venom-induced hyperalgesia was blocked by the bradykinin B-2 receptor antagonist HOE 140. On the other hand, des-Arg(9), [Leu(8)]-bradykinin, a bradykinin B-1 receptor antagonist, did not modify the hyperalgesic response. These results suggest that bradykinin, acting on B-2 receptor, is a mediator of hyperalgesia induced by B. jararaca venom.
机译:缓激肽参与了由Botrops jararaca蛇毒-足内注射B. jararaca蛇毒(5杯/爪)引起的大鼠痛觉过敏的痛觉过敏(痛觉过敏),在毒液注射后1 h达到峰值。异丙嗪,(H-1受体拮抗剂),甲基麦角酰胺(5-HT受体拮抗剂),胍乙啶(交感神经功能抑制剂),抗TNF-α或抗白介素1抗体或螯合剂CaNa都不能改变这种现象。 (2)EDTA。缓激肽B-2受体拮抗剂HOE 140阻止了由毒液引起的痛觉过敏。另一方面,缓激肽B-1受体拮抗剂des-Arg(9),[Leu(8)]-缓激肽并未改变该药物的痛觉过敏。痛觉过敏反应。这些结果表明,作用于B-2受体的缓激肽是由jararaca毒液诱导的痛觉过敏的介体。

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