Messlinger K, Schepelmann K, Pawlak M, Schmidt R F
Physiologisches Institut, Universität Würzburg, Germany.
Neurosci Lett. 1993 Dec 24;164(1-2):21-4. doi: 10.1016/0304-3940(93)90847-e.
Arthritic hyperalgesia and pain result from an increased activity of nociceptive afferents that may be induced and maintained by inflammatory mediators like bradykinin (BK). The B1 receptor antagonist des-Arg9-Leu8-BK and the B2 receptor antagonists Thi5,8-D-Phe7-BK and Hoe 140 were used to study the involvement of BK receptors in the generation of ongoing afferent activity in the cat's knee joint that was inflamed by kaolin and carrageenin. After i.a. bolus administration of BK receptor antagonists (26-260 micrograms) close to the joint, the ongoing activity did not significantly vary in any group III or group IV unit. We conclude that activation of BK receptors by endogenous BK is probably not the mechanism that is responsible for the increased ongoing activity of articular afferents in the inflamed joint.
关节炎性痛觉过敏和疼痛是由伤害性传入神经活动增加引起的，这种增加可能由缓激肽（BK）等炎症介质诱导并维持。使用B1受体拮抗剂去-精氨酸9-亮氨酸8-缓激肽以及B2受体拮抗剂噻吩5,8-二苯丙氨酸7-缓激肽和Hoe 140，来研究BK受体在高岭土和角叉菜胶致炎的猫膝关节中持续传入活动产生过程中的作用。在关节附近经关节内推注给予BK受体拮抗剂（26 - 260微克）后，III类或IV类单位的持续活动在任何组中均无显著变化。我们得出结论，内源性BK激活BK受体可能不是导致炎症关节中关节传入神经持续活动增加的机制。
