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首页> 外文期刊>The Open Pain Journal >Dual Roles for Endothelin-B Receptors in Modulating Adjuvant-Induced Inflammatory Hyperalgesia in Rats
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Dual Roles for Endothelin-B Receptors in Modulating Adjuvant-Induced Inflammatory Hyperalgesia in Rats

机译：内皮素-B受体在调节佐剂诱导的大鼠炎性痛觉过敏中的双重作用。

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Injection of endothelin-1 (ET-1) into the plantar rat hindpaw causes acute pain at high concentrations and tactile sensitization at low concentrations. The pro-nociceptive actions are driven through ETA receptors for both levels of [ET-1], but the ETB receptors are only pro-nociceptive for allodynia from low [ET-1] and anti-nociceptive for pain from high [ET-1]. The goal of the present work was to discriminate the roles of the ET receptors in the acute hyperalgesia from inflammation by complete Freund’s adjuvant (CFA, 20 mg/paw) into the rat hindpaw. Selective antagonists were injected l0 min before and then together with CFA. An ETA receptor antagonist, BQ-123, reduced CFA-induced thermal hyperalgesia (by up to 50%), as did an ETB receptor antagonist, BQ-788 (by up to 66%). BQ-123 and BQ-788 also delayed the onset (by 1.5 – 2 h) but insignificantly reduced the maximum degree of CFA-induced allodynia (~10%). Surprisingly, an ETB receptor agonist, IRL-1620, also reduced maximum thermal hyperalgesia induced by CFA, suppressed peak allodynia and delayed its occurrence by ~ 3 h. The latter actions of IRL-1620 were reversed by coadministration of BQ-788, naloxone hydrochloride and the peripherally restricted opiate receptor antagonist naloxone methiodide, and by antiserum against β-endorphin. These findings demonstrate an important role for endogenous ET-1 in acute inflammatory pain and a dual action of ETB receptors, including a pro-algesic action along with the important activation of a local analgesic pathway, implying that at least two different ETB receptors contribute to modulation of inflammatory pain.
机译：在足底大鼠后爪中注射内皮素-1（ET-1）会导致高浓度的急性疼痛和低浓度的触觉致敏。 ETA受体对两种水平的[ET-1]均具有伤害伤害感受的作用，但ETB受体仅在[ET-1]较低时对痛觉过敏具有伤害感受作用，而在[ET-1]较高时对疼痛具有抗伤害感受作用]。本研究的目的是通过完全弗氏佐剂（CFA，20 mg / paw）进入大鼠后爪来区分ET受体在急性痛觉过敏中的作用与炎症。在10分钟之前注射选择性拮抗剂，然后与CFA一起注射。 ETA受体拮抗剂BQ-123减少了CFA诱导的热痛觉过敏（最多降低了50％），而ETB受体拮抗剂BQ-788减少了CFA引起的热痛觉过敏（最多降低了66％）。 BQ-123和BQ-788也延迟了发病时间（1.5 – 2小时），但并未显着降低CFA诱发的异常性疼痛的最大程度（〜10％）。出乎意料的是，ETB受体激动剂IRL-1620也减少了CFA引起的最大热痛觉过敏，抑制了峰值异常性疼痛并将其发生延迟了约3小时。 BQ-788，盐酸纳洛酮和外围受限制的阿片受体拮抗剂纳洛酮甲硫醇并用抗β-内啡肽的抗血清可逆转IRL-1620的后一作用。这些发现表明内源性ET-1在急性炎性疼痛和ETB受体的双重作用（包括促镇痛作用以及局部镇痛途径的重要激活）中起着重要作用，这意味着至少有两种不同的ETB受体促成调节炎症性疼痛。

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