Kinins are small peptides produced rapidly following tissue injury that serve as important modulators of inflammation and pain. In the periphery, the actions of kinins include vasodilatation, increased vascular permeability, stimulation of immune cells, and induction of pain. Kinins in the central nervous system (CNS) seem to initiate a similar cascade of events leading to neural tissue damage, as well as long lasting disturbances affecting blood-brain barrier function.¹

Kinins, such as Bradykinin (BK), Lys-BK, desArg⁹-BK, and Lys-desArg⁹-BK, exert their action via two distinct receptors: the B₁ Bradykinin receptor (BKRB1) and the B₂ Bradykinin receptor (BKRB2). BKRB2 is activated by BK and Lys-BK while desArg⁹-BK and Lys-desArg⁹-BK activate BKRB1.²  Activation of BKRB2 liberates mediators of vascular tone, fibrinolysis, and pain. BKRB2, which mediates most of the physiological effects of kinins, as well as BKRB1, represent potential therapeutic targets for treatment of inflammatory disorders and cardiovascular diseases.

Both BKRB1 and BKRB2 are members of the seven-transmembrane domain, G protein-coupled receptor (GPCR) superfamily and share a common structure of seven putative transmembrane domains, an extracellular amino terminus, and a cytoplasmic carboxy terminus.

BKRB2 is constitutively and widely expressed throughout the CNS and peripheral nervous system and on various cell types including endothelial cells, nerve fibers, leukocytes, and mast cells.^3-5