Dray A
Astra Research Centre Montreal, QC, Canada.
Can J Physiol Pharmacol. 1997 Jun;75(6):704-12.
Kinins (bradykinin, kallidin) are produced at sites of injury and inflammation and serve a critical role in signaling tissue distress as well as organising tissue responsiveness to injury. The acute activation and prolonged sensitization of fine afferents, to produce pain and hyperalgesia, are important in the protective responses that occur to minimize further tissue injury. These effects occur via activation of B2 receptors present on sensory neurons, resulting in a change of membrane excitability and altered cellular neurochemistry. B2 receptor activation of a variety of tissues including postganglionic sympathetic fibres stimulates the production of several proinflammatory mediators, including prostanoids and cytokines, which interact with kinins and contribute to inflammation and hyperalgesia. Increased expression of B1 receptors plays a prominent role in inflammatory hyperalgesia, but further characterization of the cellular mechanism is required. A role for kinins and kinin receptors in central pathophysiologies (trauma, ischemia, infection) needs examination. The evidence for modulation of nociception and central pain generation is compelling, as central bradykinin administration causes hyperalgesia, whereas B2 antagonists are antinociceptive. The basis for these effects should be urgently investigated. Such data will add further support to the utilization of bradykinin receptor antagonists for the treatment of peripheral and central pain.
激肽（缓激肽、胰激肽）在损伤和炎症部位产生，在传递组织损伤信号以及组织机体对损伤的反应方面发挥关键作用。细传入神经的急性激活和长期致敏以产生疼痛和痛觉过敏，在发生的保护性反应中很重要，可将进一步的组织损伤降至最低。这些效应通过激活感觉神经元上的B2受体而发生，导致膜兴奋性改变和细胞神经化学变化。包括节后交感神经纤维在内的多种组织的B2受体激活会刺激多种促炎介质的产生，包括前列腺素和细胞因子，这些介质与激肽相互作用并导致炎症和痛觉过敏。B1受体表达增加在炎性痛觉过敏中起重要作用，但需要进一步明确其细胞机制。激肽和激肽受体在中枢病理生理学（创伤、缺血、感染）中的作用有待研究。伤害感受和中枢性疼痛产生受调制的证据很有说服力，因为中枢给予缓激肽会导致痛觉过敏，而B2拮抗剂具有抗伤害感受作用。应迫切研究这些效应的基础。这些数据将进一步支持使用缓激肽受体拮抗剂治疗外周和中枢性疼痛。
