Department of Pharmacology and Physiology, School of Pharmaceutical Sciences, Universiti Sains Malaysia, 11800, Penang, Malaysia.
Inflammopharmacology. 1998;6(4):289-96. doi: 10.1007/s10787-998-0013-5.
Components of the kallikrein-kinin system are activated in response to noxious stimuli (chemical, physical or bacterial), which may lead to excessive release of kinins in the synovial joints that may produce inflammatory joint disease. The inflammatory changes observed in synovial tissue may be due to activation of B(2) receptors. Kinins also stimulate the synthesis of other pro-inflammatory agents (PGs, LTs, histamine, EDRF, PGI(2) and PAF) in the inflamed joint. B(2)-receptor antagonists may provide valuable agents as new analgesic drugs. Furthermore, it is suggested that substances to reduce activation of the kallikrein-kinin system (KKS) may provide a pharmacological basis for the synthesis of novel antirheumatic or anti-inflammatory drugs.
激肽释放酶-激肽系统的成分被激活以响应有害刺激（化学、物理或细菌），这可能导致滑液关节中激肽的过度释放，从而产生炎症性关节疾病。在滑膜组织中观察到的炎症变化可能是由于 B(2)受体的激活。激肽还刺激在炎症关节中其他促炎剂（PGs、LTs、组胺、EDRF、PGI(2)和 PAF）的合成。B(2)-受体拮抗剂可能作为新型镇痛药提供有价值的药物。此外，有人认为，减少激肽释放酶-激肽系统（KKS）激活的物质可能为合成新型抗风湿或抗炎药物提供药理学基础。
