Bradykinin
Bradykinin is a 9-aa vasoactive peptide from the kinin-kallikrein system that produces vasodilation, increases vascular permeability, and sensitizes pain nociceptors. Central to ACE inhibitor-induced angioedema and inflammation research.
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Compound Profile
Bradykinin
Key Data
Research reference only
Research Focus
Preclinical data
⚠ Research & Educational Use Only. Bradykinin is a research chemical documented here for scientific education. All information references peer-reviewed literature and preclinical/clinical study data. Not for human consumption. Not medical advice. Consult a licensed researcher or healthcare professional before any laboratory use.
- Potent endogenous vasodilator via B2R → eNOS activation → nitric oxide production in endothelium
- Cardioprotective: bradykinin accumulation contributes to ACE inhibitor-mediated cardiovascular benefit
- Anti-inflammatory via B1R and B2R in resolution of inflammation studies
- Bradykinin is not FDA-approved for human use. It is a research chemical for scientific study only.
Research At a Glance
- Potent endogenous vasodilator via B2R → eNOS activation → nitric oxide production in endothelium
- Cardioprotective: bradykinin accumulation contributes to ACE inhibitor-mediated cardiovascular benefit
- Anti-inflammatory via B1R and B2R in resolution of inflammation studies
- Key mediator of ischemic preconditioning — bradykinin B2R activation is required for cardioprotection during brief ischemia
In Plain English
Simple summaryBradykinin is a 9-amino acid peptide generated in blood plasma during tissue injury, inflammation, and allergic reactions through the kinin-kallikrein cascade. It's not stored -- it's produced on demand when kallikrein enzymes cleave kininogens in plasma. Bradykinin causes vasodilation, increases vascular permeability (the leakiness that causes swelling), stimulates pain receptors, and triggers bronchoconstriction. It's most clinically relevant through two negative effects: the cough that ACE inhibitors cause (ACE normally degrades bradykinin, so ACE inhibitors let bradykinin accumulate in the airways), and hereditary angioedema (HAE), where bradykinin accumulates due to C1-inhibitor deficiency and causes potentially life-threatening swelling. HAE treatments blocking bradykinin (icatibant, berotralstat) are now approved.
- Potent endogenous vasodilator via B2R → eNOS activation → nitric oxide production in endothelium
- Cardioprotective: bradykinin accumulation contributes to ACE inhibitor-mediated cardiovascular benefit
- Anti-inflammatory via B1R and B2R in resolution of inflammation studies
The full scientific detail, mechanisms, citations, and dosing data, follows below.
What is Bradykinin?
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Bradykinin is a 9-amino acid (Arg-Pro-Pro-Gly-Phe-Ser-Pro-Phe-Arg) vasoactive kinins peptide generated from kininogen precursors by kallikrein serine proteases. High-molecular-weight kininogen (HMWK) → bradykinin via plasma kallikrein; low-molecular-weight kininogen (LMWK) → kallidin (bradykinin extended by an N-terminal Lys) via tissue kallikrein.
Bradykinin's biological effects are mediated through two G-protein-coupled receptors
- **B1R (kinin receptor 1)**: Constitutively low expression; markedly upregulated by inflammation (IL-1β, TNF-α); binds des-Arg9-bradykinin (the carboxypeptidase metabolite) preferentially
- **B2R (kinin receptor 2)**: Constitutively expressed; binds native bradykinin with high affinity → mediates acute effects
**Key physiological and pharmacological roles:**
1. **Vasodilation and blood pressure**: B2R activation on endothelial cells → eNOS activation → NO production → smooth muscle relaxation. This is why ACE inhibitors lower blood pressure: ACE normally degrades bradykinin, so ACE inhibition leads to bradykinin accumulation → enhanced vasodilation.
2. **ACE inhibitor pharmacology**: The cardiovascular benefit of ACE inhibitors extends beyond Ang II suppression — studies show that B2R blockade abolishes approximately 30-50% of ACE inhibitor's antihypertensive effect. Bradykinin-dependent mechanisms also contribute to ACE inhibitor-mediated cardioprotection in post-MI patients (CONSENSUS, GISSI-3 trials context).
3. **Hereditary Angioedema (HAE)**: HAE type 1 and 2 are caused by deficiency or dysfunction of C1-esterase inhibitor, leading to unregulated plasma kallikrein activity → massive bradykinin production → severe subcutaneous and submucosal edema. The standard of care for HAE attacks now includes icatibant (selective B2R antagonist), ecallantide (kallikrein inhibitor), and lanadelumab (prophylactic kallikrein antibody).
4. **Pain**: Bradykinin is one of the most potent endogenous pain-producing compounds. B1R and B2R activation sensitizes peripheral nociceptors via PLC → IP3 → Ca2+ release → TRPV1 sensitization. This peripheral sensitization contributes to inflammatory hyperalgesia.
5. **Ischemic preconditioning**: Brief ischemia → bradykinin release → B2R → PKC activation → protective cardioprotective signaling (similar to opioid preconditioning).
By the Numbers
Key Research Benefits
Documented effects observed in preclinical and clinical studies on Bradykinin. See all Healing & Recovery peptides for comparison.
Side Effects & Risks
Adverse effects reported in the research literature. All data sourced from preclinical and clinical study reports. View all peptides' side effects →
Dosing Data from the Literature
Doses referenced below are sourced from published preclinical and clinical studies. Use the peptide dose calculator to convert these values to injection volume.
Bradykinin is used as a research tool in vascular biology and pain research:
IV infusion for endothelial function studies: 100-1000 pmol/min/100 mL forearm blood flow Intra-arterial injection: 3.2-32 nmol for dose-response studies of vasodilation Pain research: Intradermal injection at 0.1-10 nmol/site for nociceptor sensitization Angioedema models: Bradykinin receptor B2R (Icatibant) and kallikrein inhibitors (Ecallantide) are the translational research focus
Administration in Research Settings
Standard reconstitution and administration methodology for laboratory research use.
Used as a research peptide for vascular, pain, and inflammation studies. Requires fresh preparation due to extreme lability in plasma (kininases, ACE, carboxypeptidases degrade it within seconds).
What the research doesn't show
Bradykinin is primarily studied as something to block (in ACE inhibitor cough and HAE) rather than something to supplement. Its effects are largely pro-inflammatory and pro-edema in the context of injury -- the natural signal is appropriate for promoting healing locally, but its accumulation in diseases like HAE is dangerous. Understanding bradykinin biology is more useful for understanding ACE inhibitor side effects than for any direct supplementation application.
Medical Expert Videos
Physicians, researchers, and pharmacologists explain Bradykinin, covering mechanisms of action, clinical context, and study findings.
Videos sourced from YouTube search. KnowYourPeptide does not endorse any individual creator. For research education only.
The Bottom Line
Bradykinin has a growing body of preclinical evidence and a well-characterised safety profile in research settings. The most-studied application is: potent endogenous vasodilator via b2r → enos activation → nitric oxide production in endothelium.
The most commonly reported side effect in research subjects is pain sensitization — bradykinin b1r and b2r activate nociceptors and sensitize them to thermal and mechanical stimuli. It is a research chemical, not approved for human use.
Frequently Asked Questions
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Quick Reference
How It Compares
CGRP is another pain and vasodilation mediator from sensory neurons -- both contribute to neurogenic inflammation but through different receptor systems. Substance P co-localizes with bradykinin in pain signaling. Angiotensin II and bradykinin are directly linked through ACE: ACE converts angiotensin I to angiotensin II (raising blood pressure) while simultaneously degrading bradykinin (a vasodilator). ACE inhibitors shift both balances simultaneously.
Compare Bradykinin side-by-sideResearch Use Only
This information is for educational research purposes only. This is not medical advice. Consult a qualified healthcare professional.