Bradykinin B2 Receptor (B2R)

Bradykinin B2 receptor (B2R) mediates common kinin responses, including hypotension, bronchoconstriction, epithelial secretion, vascular permeability, pain, cytokine release, and eicosanoid formation^[1]. Mechanistically, bradykinin-induced B2R activation drives vasodilation in human forearm resistance vessels, and icatibant dose-dependently inhibits this B2R-mediated vascular response^[2]. In airway inflammation models, B2R blockade with icatibant reduces antigen-induced nasal hyperresponsiveness, eosinophils, eosinophil cationic protein, kinin, and IL-8 in seasonal allergic rhinitis^[3]. In hereditary angioedema, bradykinin acts as the key mediator of symptoms, and the selective B2R antagonist icatibant provides clinically significant symptom relief in acute cutaneous or abdominal attacks^[4]. Compared with B1 receptor, which is inducible after injury and inflammation, B2R represents the common kinin receptor subtype and remains central to acute bradykinin signaling^[1][5]. For experimental applications, icatibant is useful for testing B2R-dependent vascular leakage and inflammatory responses, although micromolar icatibant can inhibit aminopeptidase N and alter B1 or angiotensin receptor signaling^[6].