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Research Only Cardiovascular & Renal

Bradykinin

also known as: BK, Kallidin, Kinin-9

The vasoactive peptide behind ACE inhibitor cough — an endogenous inflammatory mediator that connects cardiovascular pharmacology to angioedema, pain, and allergic responses.

A 9-amino-acid vasoactive peptide generated by kallikrein cleavage of kininogen that produces vasodilation, increases vascular permeability, and causes pain via B1 and B2 receptors — accumulated by ACE inhibitors and antagonized by icatibant for hereditary angioedema.

Mechanism of action

Generated by plasma kallikrein from high-molecular-weight kininogen. Binds B2 receptors (constitutive, Gq-coupled) causing vasodilation via endothelial NO and prostacyclin release, increased vascular permeability, and nociceptor activation. B1 receptors (inducible, upregulated in inflammation) mediate sustained inflammatory pain. Degraded primarily by ACE.

Primary uses

  • Endogenous vasodilation and blood pressure regulation
  • Inflammatory pain and edema signaling
  • Pharmacological target: ACE inhibitors increase BK levels
  • Hereditary angioedema pathophysiology

Typical dosing

N/A N/A N/A (endogenous)

Not used as a drug. Clinical relevance is through modulation of its pathway.

Regulatory status

Bradykinin itself is not a drug, but its pathway is the target of: ACE inhibitors (block BK degradation), icatibant (Firazyr, B2R antagonist for HAE, approved 2011), and lanadelumab (Takhzyro, anti-kallikrein antibody).

References

  1. [review] Marceau F, Regoli D. "Bradykinin receptor ligands: therapeutic perspectives." Nat Rev Drug Discov. 2004;3(10):845-852.
  2. [pubmed] Garvin MR, et al. "A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm." eLife. 2020;9:e59177.

Related peptides

Angiotensin II

Giapreza — the first new vasopressor class approved in decades. FDA-approved December 2017 (La Jolla Pharmaceutical) for catecholamine-resistant septic / distributive shock based on the ATHOS-3 trial (NEJM 2017, n=321). Engages a third vasoconstrictor pathway (RAAS / AT1) independent of catecholamines and vasopressin — useful when both of those axes are desensitised.

Icatibant

The bradykinin blocker for angioedema — a synthetic decapeptide B2 receptor antagonist that stops acute swelling attacks within 30 minutes.

ANP

The atrial pressure sensor — the first discovered natriuretic peptide, maintaining blood pressure and fluid balance through renal sodium excretion and vasodilation.

BNP

The heart failure biomarker — an endogenous cardiac peptide whose blood levels are the gold standard for diagnosing and monitoring heart failure severity.

Vasopressin

Vasostrict — the endogenous antidiuretic hormone as an ICU vasopressor. FDA-approved April 2014 for adults with vasodilatory shock (post-cardiotomy, sepsis) who remain hypotensive despite fluids and catecholamines. Works through V1a receptors on vascular smooth muscle — a receptor axis pharmacologically distinct from catecholamine receptors, preserving its vasopressor effect when adrenergic receptors are desensitised.

Guides & tools

Disclaimer

This entry is for educational purposes only and does not constitute medical advice. Dosing information reflects published regulatory or research data and is not a recommendation. Many compounds described here are not approved for human use in the United States. Consult a licensed medical professional before considering any peptide therapy.