Involvement of the kallikrein-kinin system in a model of hyperalgesia in low kallikrein rats

摘要

Bradykinin (BK) is one of the primary mediators of pain and inflammation. It is released in damaged tissue by kininogen precursors through kallikrein action and rapidly inactivated by proteolytic enzymes. BK exerts its effects by activating specific receptors named B_1 and B_2. B_2 receptors are constitutively and widely expressed in tissues, whereas B_1 receptors are not usually expressed under physiological conditions but can be induced by various mediators. The synthesis of selective, competitive BK-antagonists and the production of knockout mice for B_1 and B_2 receptors have enabled better clarification of the role of these receptors, in spite of discordant opinions on their involvement in the pain response.