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Bradykinin is a potent vasoactive nonapeptide that plays a central role in inflammation, vasodilation, increased vascular permeability, and pain signaling. It is generated from high-molecular-weight kininogen by the action of kallikrein enzymes as part of the kinin–kallikrein system.
Bradykinin exerts its effects primarily through two G protein-coupled receptors: B2 Receptor (constitutively expressed) and B1 Receptor (induced during inflammation or tissue injury). Neutralizing bradykinin can be achieved by inhibiting its synthesis (e.g., blocking kallikrein activity), enhancing its degradation (e.g., increasing carboxypeptidase N activity), or blocking receptor binding (using B2 receptor antagonists).
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