Nagy I, Paule C, White J, Urban L
Department of Anaesthetics, Pain Medicine and Intensive Care, Imperial College London, London, UK.
Br J Pharmacol. 2007 Jul;151(6):721-2. doi: 10.1038/sj.bjp.0707274. Epub 2007 May 29.
While the role of the brain kallikrein-kinin system in the development of various pathological processes, such as oedema formation following brain injury or induction of central hypertonia has generated major interest, the possible role of this system in nociceptive processing has received little attention. In their present paper, Mortari et al. (2007) show that bradykinin B2 receptor activation in the brain by the bradykinin analogue, Thr(6)-bradykinin, isolated from the venom of the social wasp, Polybia occidentalis potently reduces acute, noxious heat-evoked reflex responses in naive rats. The unknown underlying mechanism of this powerful antinociceptive effect reminds us that the supraspinal antinociceptive system is still a "black box" in many aspects and awaits thorough investigation.
尽管脑激肽释放酶-激肽系统在各种病理过程的发展中所起的作用,如脑损伤后的水肿形成或中枢性高血压的诱发,已引起了人们的极大兴趣,但该系统在伤害性感受处理中的可能作用却很少受到关注。在他们目前的论文中,莫塔里等人(2007年)表明,从西方社会性黄蜂多刺蚁毒液中分离出的缓激肽类似物苏氨酸(6)-缓激肽激活脑中的缓激肽B2受体,能有效降低未接触过该物质的大鼠急性、有害热诱发的反射反应。这种强大的抗伤害感受作用的潜在机制尚不清楚,这提醒我们,脊髓上抗伤害感受系统在许多方面仍是一个“黑匣子”,有待深入研究。