Bradykinin receptor B1; Bradykinin receptor B2 (B1R; B2R)

Bradykinin receptors B1 and B2 are members of the G protein-coupled receptor (GPCR) family that mediate the biological effects of kinins in the kallikrein-kinin system. The B2 receptor is constitutively and ubiquitously expressed in most healthy tissues, mediating physiological effects such as vasodilation, increased vascular permeability, smooth muscle changes, and pain. In contrast, the B1 receptor is inducible and is upregulated in response to tissue injury, inflammation, or the presence of proinflammatory cytokines, playing a key role in pathological pain and inflammatory responses. Both receptors are seven-transmembrane proteins that activate G proteins—primarily G_q for B2—leading to downstream signaling events including phospholipase C activation, intracellular calcium mobilization, MAP kinase pathway stimulation, and modulation of various cellular processes. B2 is targeted by drugs such as icatibant for hereditary angioedema, while B1 is an emerging target for chronic inflammation and pain syndromes. The two receptors differ in ligand specificity: B2 binds bradykinin and kallidin, while B1 preferentially binds their des-Arg derivatives[1][3][4][6][7].

Other names

B1 bradykinin receptorB2 bradykinin receptorB1RB2RKinin B1 receptorKinin B2 receptor

B2 antagonists block bradykinin-mediated vasodilation and vascular permeability B1 antagonists block inflammation-induced responses such as pain and vascular leakage Agonists or antagonists modulate G_q and G_i signaling (PLC activation, calcium release, MAP kinase activation)