Steranka L R, Manning D C, DeHaas C J, Ferkany J W, Borosky S A, Connor J R, Vavrek R J, Stewart J M, Snyder S H
Nova Pharmaceutical Corporation, Baltimore, MD 21224.
Proc Natl Acad Sci U S A. 1988 May;85(9):3245-9. doi: 10.1073/pnas.85.9.3245.
Autoradiographic studies localize [3H]bradykinin receptor binding sites to the substantia gelatinosa, dorsal root, and a subset of small cells in both the dorsal root and trigeminal ganglia of the guinea pig. [3H]Bradykinin labeling is also observed over myocardial/coronary visceral afferent fibers. The localization of [3H]bradykinin receptors to nociceptive pathways supports a role for bradykinin in pain mediation. Several bradykinin antagonists block bradykinin-induced acute vascular pain in the rat. The bradykinin antagonists also relieve bradykinin- and urate-induced hyperalgesia in the rat paw. These results indicate that bradykinin is a physiologic mediator of pain and that bradykinin antagonists have analgesic activity in both acute and chronic pain models.
放射自显影研究将[3H]缓激肽受体结合位点定位到豚鼠的脊髓胶状质、背根以及背根神经节和三叉神经节中的一小部分小细胞。在心肌/冠状内脏传入纤维上也观察到[3H]缓激肽标记。[3H]缓激肽受体在伤害性感受通路中的定位支持了缓激肽在疼痛介导中的作用。几种缓激肽拮抗剂可阻断大鼠中缓激肽诱导的急性血管性疼痛。缓激肽拮抗剂还可减轻大鼠爪中缓激肽和尿酸盐诱导的痛觉过敏。这些结果表明,缓激肽是疼痛的生理介质,并且缓激肽拮抗剂在急性和慢性疼痛模型中均具有镇痛活性。