新生大鼠体外模型中周围神经和脊髓缓激肽受体的激活
Activation of a bradykinin receptor in peripheral nerve and spinal cord in the neonatal rat in vitro.
作者信息
Dray A, Bettaney J, Forster P, Perkins M N
机构信息
Sandoz Institute for Medical Research, London.
出版信息
Br J Pharmacol. 1988 Dec;95(4):1008-10. doi: 10.1111/j.1476-5381.1988.tb11732.x.
Abstract
In an in vitro preparation of the neonatal rat spinal cord with attached tail, administration of bradykinin (Bk) to the spinal cord or to the tail produced depolarization of a ventral root (L3-L5). The effect of Bk at each site was selectively and reversibly antagonized by D-Arg [Hyp2, Thi5,8 D-Phe7]-Bk but could not be mimicked or antagonized by the B1-receptor ligands [des-Arg9]-Bk or Leu8[des-Arg9]-Bk, respectively. Peripherally evoked noxious responses produced by capsaicin or heat, were unaffected by either antagonist administered to the spinal cord. These data suggest that Bk-evoked responses in the spinal cord and at peripheral nociceptors were mediated via a receptor which by definition is of the B2-type. Additionally Bk is unlikely to be a physiological mediator of acute nociception in the spinal cord.
摘要
在带有尾巴的新生大鼠脊髓的体外制备物中，向脊髓或尾巴施用缓激肽（Bk）会导致腹根（L3 - L5）去极化。D - Arg [Hyp2, Thi5,8 D - Phe7] - Bk可选择性且可逆地拮抗Bk在每个部位的作用，但B1受体配体[des - Arg9] - Bk或Leu8[des - Arg9] - Bk分别无法模拟或拮抗其作用。辣椒素或热引起的外周诱发伤害性反应，不受施用于脊髓的任何一种拮抗剂的影响。这些数据表明，脊髓和外周伤害感受器中Bk诱发的反应是通过一种根据定义属于B2型的受体介导的。此外，Bk不太可能是脊髓中急性伤害感受的生理介质。
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本文引用的文献
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Bradykinin analogue blocks bradykinin-induced inhibition of a spinal nociceptive reflex in the rat.缓激肽类似物可阻断缓激肽诱导的大鼠脊髓伤害性反射抑制。
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New synthetic antagonists of bradykinin.缓激肽的新型合成拮抗剂。
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