BRADYKININ-INDUCED KNEE-JOINT INCAPACITATION INVOLVES BRADYKININ B-2 RECEPTOR-MEDIATED HYPERALGESIA AND BRADYKININ B-1 RECEPTOR-MEDIATED NOCICEPTION

The participation of B-1 and B-2 types of bradykinin receptors was stu died in the rat knee-joint incapacitation test. Five intra-articular s uccessive hourly administrations of bradykinin produced progressive in capacitation, thus indicating that bradykinin induced sensitization to its own nociceptive effect. Four co-injections of bradykinin with the bradykinin B-1 receptor antagonist des-Arg(9)-[Leu(8)]bradykinin were without nociceptive effect. However, a 5th injection of bradykinin al one produced intense incapacitation. The bradykinin B, receptor antago nist HOE-140 [D-Arg(0)[Hyp(3),Thi(5),D-TiC7,OiC(8)]bradykinin), or ind omethacin, prevented the bradykinin-induced incapacitation. However, s uccessive co-injections of bradykinin with prostaglandin E-2, in contr ast to bradykinin alone, did induce incapacitation in animals pretreat ed with indomethacin or HOE-140. The injection of the bradykinin B-1 r eceptor agonist des-Arg(9)-bradykinin into prostaglandin E-2-treated j oints did induce incapacitation, although administration of the bradyk inin B-1 receptor agonist or prostaglandin E-2 alone did not induce in capacitation. In conclusion, in ongoing articular inflammation, it is suggested that the bradykinin B-2 receptor is particularly involved wi th nociceptor activation, while the bradykinin B-2 receptor is related to nociceptor sensitization.