Bradykinin

Cardiovascular / Inflammation

Also known as: BK, Kallidin, Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg

KininsResearch phase: Endogenous peptide (well characterized)Regulatory: Endogenous peptide. Icatibant (B2R antagonist) is FDA-approved for hereditary angioedema. ACE inhibitors work partly by potentiating bradykinin.

Mechanism

Bradykinin is a 9-amino-acid peptide that causes blood vessels to dilate, blood pressure to drop, and pain/inflammation to increase. It is produced by the kallikrein-kinin system during tissue injury and inflammation. Bradykinin is famously responsible for the dry cough side effect of ACE inhibitor blood pressure medications, because ACE normally breaks down bradykinin.

Technical detail

Bradykinin (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) is a vasoactive nonapeptide generated from high-molecular-weight kininogen (HMWK) by kallikrein. It acts on B2 receptors (constitutive, Gq-coupled) to activate PLC-IP3-DAG, increasing intracellular Ca2+ in endothelial cells, stimulating eNOS (NO production), COX-1/2 (prostacyclin release), and EDHF release for vasodilation. B1 receptors (inducible by inflammation) are activated by des-Arg9-bradykinin. ACE (kininase II) is the primary degradation enzyme, explaining why ACE inhibitors potentiate bradykinin effects (cough, angioedema). Also activates sensory nerve C-fibers via TRPV1 for pain signaling.

Evidence

Bradykinin receptors: Agonists, antagonists, expression, signaling, and adaptation to sustained stimulation
François Marceau et al. (2020) — International Immunopharmacology — PMID: 32106060
Review summarizes B1/B2 bradykinin receptor biology and notes that icatibant, a peptide B2 receptor antagonist, is an approved therapy for hereditary angioedema, positioning bradykinin-system modulation as a clinically relevant therapeutic pathway.
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