What it is
Bradykinin is a peptide of nine amino acids — RPPGFSPFR. The body does not make it as a free hormone. It is cut out of a much larger blood protein, kininogen-1, which UniProt (P01042) records at 644 residues; bradykinin is residues 381 to 389. The cutting is done by enzymes called kallikreins, which switch on when tissue is injured or inflamed.
A one-residue-longer version, kallidin (lysyl-bradykinin, KRPPGFSPFR), is cut from the same spot; both are called kinins.
How it was found
The name comes from a 1949 paper in the American Journal of Physiology by Rocha e Silva, Beraldo and Rosenfeld (PMID 18127230). Adding venom of the jararaca pit viper — or the digestive enzyme trypsin — to a fraction of blood plasma released something that lowered blood pressure and made gut muscle contract slowly. Hence brady- (slow) and -kinin (movement).
The same snake reappears later in the story. In 1965 Ferreira reported a "bradykinin potentiating factor" in jararaca venom — something that made bradykinin's effects stronger and longer (Experientia, PMID 5870517).
What it does
UniProt's annotation, summarising the literature, lists bradykinin's effects:
| Effect | What it means |
|---|---|
| Widens blood vessels | Lowers blood pressure locally and overall |
| Makes vessels leaky | Fluid and immune cells cross into tissue — swelling |
| Stimulates pain nerves | One of the signals behind inflammatory pain |
| Releases other mediators | Such as prostaglandins, which amplify inflammation |
| Increases salt and water loss | Through the kidney |
It acts mainly through two receptors, B1 and B2, and is broken down within moments by several enzymes — ACE chief among them.
Two places medicine meets it
ACE inhibitors. The captopril label states plainly that ACE "is identical to 'bradykininase'", and that captopril "may also interfere with the degradation of the vasodepressor peptide, bradykinin" — so higher bradykinin levels may contribute to how the drug works. Bradykinin's role in the dry cough and the rarer facial swelling linked to this drug class is widely discussed in the literature; this entry records the mechanism the label states, and any symptom on a prescribed drug belongs with the prescriber.
Hereditary angioedema. The icatibant label (Firazyr) gives the mechanism: when the control protein C1-esterase inhibitor is absent or faulty, the kallikrein cascade overproduces bradykinin, which is thought to cause the localised swelling, inflammation and pain of an attack. Icatibant is itself a peptide — a synthetic decapeptide carrying five non-standard amino acids — that blocks the B2 receptor with an affinity similar to bradykinin's own. Drugs@FDA dates Firazyr (NDA 022150) to 2011-08-25; generic icatibant followed from 2020.
Where it stands
openFDA's Drugs@FDA returns no application with bradykinin itself as the active ingredient (2026-10-02). PubMed returns 23,025 records for bradykinin, 307 tagged as randomised controlled trials — a large literature, almost all of it about bradykinin as a signal to measure or block rather than as something to give.
Related reading
Bradykinin belongs with the library's other inflammation signals — see peptides for inflammation — and with the blood-pressure peptides vasopressin and the natriuretic peptides in BNP and NT-proBNP. Like hepcidin and somatostatin, it is recorded here as one of the body's own peptides, so the drugs built around it make sense.