Burch R M, DeHaas C
Nova Pharmaceutical Corporation, Baltimore, Maryland 21224.
Naunyn Schmiedebergs Arch Pharmacol. 1990 Aug;342(2):189-93. doi: 10.1007/BF00166963.
Bradykinin has been implicated in acute inflammatory reactions. Intradermal injection elicits increased vascular permeability and hyperalgesia, and bioassays have suggested increased bradykinin concentration in inflammatory exudates. Poorly specific inhibitors of kallikrein, the enzyme catalyzing formation of bradykinin, inhibit certain acute inflammatory reactions. However, the lack of a specific bradykinin receptor antagonist has made proof of the hypothesis difficult. In this study, we have used the potent, specific bradykinin antagonist DArg[Hyp3DPhe7] bradykinin (NPC 567) as a probe to examine the role of bradykinin in carrageenan-induced edema in the paws of rats. Subplantar injection of carrageenan led to an increase in immunoreactive bradykinin and metabolic product, desArg9bradykinin. NPC 567 inhibited the development of edema in response to carrageenan, to a maximum 65%. Thus, bradykinin appears to be a major mediator of increased vascular permeability in response to carrageenan.
缓激肽与急性炎症反应有关。皮内注射会引起血管通透性增加和痛觉过敏，生物测定表明炎症渗出物中缓激肽浓度升高。激肽释放酶（催化缓激肽形成的酶）的非特异性抑制剂可抑制某些急性炎症反应。然而，由于缺乏特异性缓激肽受体拮抗剂，这一假说的验证变得困难。在本研究中，我们使用强效、特异性缓激肽拮抗剂DArg[Hyp3DPhe7]缓激肽（NPC 567）作为探针，来研究缓激肽在角叉菜胶诱导的大鼠爪部水肿中的作用。足底注射角叉菜胶会导致免疫反应性缓激肽及其代谢产物去精氨酸9缓激肽增加。NPC 567可抑制角叉菜胶诱导的水肿发展，最大抑制率为65%。因此，缓激肽似乎是角叉菜胶引起血管通透性增加的主要介质。
