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

[review] Marceau F, Regoli D. "Bradykinin receptor ligands: therapeutic perspectives." Nat Rev Drug Discov. 2004;3(10):845-852.
[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.

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.