Bradykinin
Evidence: CCardiovascular / Vascular
Evidence Snapshot
Regulatory Context
This page summarizes research on the peptide and does not imply that the peptide is an FDA-approved drug or approved for a particular indication. Molecule-specific regulatory status requires verification against official regulatory records.
Research Takeaway
Bradykinin is a distinct kinin peptide and must not be merged with Kallidin/Lys-Bradykinin, des-Arg kinin metabolites, kininogen precursor proteins, or B1/B2 receptor drugs.
See all 6 evidence claims →Quick Summary
Bradykinin is a potent endogenous kinin peptide with extensive direct-human vascular physiology evidence. Human intra-arterial studies consistently show strong vasodilator and endothelial signaling effects, but this does not translate into established therapeutic efficacy and receptor-antagonist drug data must remain context rather than Bradykinin evidence.
Mechanism & Research Overview
Bradykinin is a potent endogenous kinin peptide with extensive direct-human vascular physiology evidence. Human intra-arterial studies consistently show strong vasodilator and endothelial signaling effects, but this does not translate into established therapeutic efficacy and receptor-antagonist drug data must remain context rather than Bradykinin evidence.
Evidence Claims
Individual scientific statements drawn from the sources cited below, each shown with the specific evidence boundary that statement does not establish.
Supported
Bradykinin is a distinct kinin peptide and must not be merged with Kallidin/Lys-Bradykinin, des-Arg kinin metabolites, kininogen precursor proteins, or B1/B2 receptor drugs.
Sources: Effect of NG-monomethyl-L-arginine on kinin-induced vasodilation in the human forearm; Bradykinin stimulates tissue plasminogen activator release from human forearm vasculature through B2 receptor-dependent, NO synthase-independent, and cyclooxygenase-independent pathway
Supported
Direct intra-arterial Bradykinin administration in healthy humans produces potent, dose-responsive forearm vasodilation.
Does not establish
Evidence boundary: These are local experimental physiology studies, not therapeutic efficacy trials.
Sources: Effect of NG-monomethyl-L-arginine on kinin-induced vasodilation in the human forearm; Local L-NG-monomethyl-arginine attenuates the vasodilator action of bradykinin in the human forearm; Bradykinin stimulates tissue plasminogen activator release from human forearm vasculature through B2 receptor-dependent, NO synthase-independent, and cyclooxygenase-independent pathway; Direct biochemical evidence for eNOS stimulation by bradykinin in the human forearm vasculature
Supported
Human studies support contributions from endothelial nitric oxide and other endothelial signaling pathways to Bradykinin-induced vasodilation.
Does not establish
Evidence boundary: Mechanistic inhibitor experiments do not imply that receptor drugs are equivalent to Bradykinin itself.
Sources: Effect of NG-monomethyl-L-arginine on kinin-induced vasodilation in the human forearm; Local L-NG-monomethyl-arginine attenuates the vasodilator action of bradykinin in the human forearm; Direct biochemical evidence for eNOS stimulation by bradykinin in the human forearm vasculature; Endothelium-derived hyperpolarizing factor mediates bradykinin-stimulated tissue plasminogen activator release in humans
Supported
Bradykinin can stimulate endothelial tissue-plasminogen-activator release in experimental human forearm studies.
Does not establish
Evidence boundary: This is endothelial physiology and does not establish Bradykinin as a clinical thrombolytic treatment.
Sources: Bradykinin stimulates tissue plasminogen activator release from human forearm vasculature through B2 receptor-dependent, NO synthase-independent, and cyclooxygenase-independent pathway; Endothelium-derived hyperpolarizing factor mediates bradykinin-stimulated tissue plasminogen activator release in humans
Supported
Clinical evidence involving icatibant or other B1/B2 receptor drugs is receptor-context evidence unless exact Bradykinin is directly administered in the same source.
Supported
No molecule-specific regulatory conclusion is frozen for native Bradykinin in Stage 2A.
Safety & Evidence Limitations
Considerations reported in the sources cited on this page — not a complete list of every possible risk, and not medical advice.
Safety Consideration
Bradykinin is a potent vasoactive mediator; hypotension, vasodilation, flushing, and related acute effects are biologically plausible.Safety Consideration
Bradykinin participates in inflammatory and permeability signaling; exact clinical risk depends strongly on route, exposure, and context.Safety Consideration
The frozen human evidence is primarily short-term local infusion physiology rather than chronic systemic safety research.
Research Areas Being Studied
Research areas discussed on this page reflect the Cardiovascular / Vascular category and the sources cited below.
Findings Reported in Studies
Educational summary only — reported in cited studies, not a claim of proven benefit.
- Endothelium-derived hyperpolarizing factor mediates bradykinin-stimulated tissue plasminogen activator release in humans (2014):
- Direct biochemical evidence for eNOS stimulation by bradykinin in the human forearm vasculature (2003):
- Bradykinin stimulates tissue plasminogen activator release from human forearm vasculature through B2 receptor-dependent, NO synthase-independent, and cyclooxygenase-independent pathway (2000):
- Effect of NG-monomethyl-L-arginine on kinin-induced vasodilation in the human forearm (1994):
- Local L-NG-monomethyl-arginine attenuates the vasodilator action of bradykinin in the human forearm (1994):
Study Tables by Evidence Type
Human Studies & Clinical Data
| Title | Year | Population / Model | Dose / Duration / Finding | Safety Notes | Source |
|---|---|---|---|---|---|
| Endothelium-derived hyperpolarizing factor mediates bradykinin-stimulated tissue plasminogen activator release in humans | 2014 | 33 healthy subjects; forearm vascular studies | Bradykinin increased tPA release and vasodilation; mechanistic blockade implicated EDHF-related pathways. | ||
| Direct biochemical evidence for eNOS stimulation by bradykinin in the human forearm vasculature | 2003 | 16 healthy volunteers; brachial artery infusion | Bradykinin dose-dependently increased forearm blood flow and biochemical indices of NO production. | ||
| Bradykinin stimulates tissue plasminogen activator release from human forearm vasculature through B2 receptor-dependent, NO synthase-independent, and cyclooxygenase-independent pathway | 2000 | Healthy volunteers; intra-arterial bradykinin with mechanistic inhibitors/antagonist | Bradykinin caused vasodilation and stimulated endothelial tPA release; B2 receptor antagonism attenuated both. | ||
| Effect of NG-monomethyl-L-arginine on kinin-induced vasodilation in the human forearm | 1994 | Healthy male volunteers; intra-arterial bradykinin | Bradykinin increased forearm blood flow; NOS inhibition partially attenuated the response. | ||
| Local L-NG-monomethyl-arginine attenuates the vasodilator action of bradykinin in the human forearm | 1994 | Healthy volunteers; brachial arterial bed | Bradykinin produced dose-dependent forearm vasodilation, attenuated by NOS inhibition. |
Animal / Cell / Preclinical Data
No Animal / Cell / Preclinical Data Listed Yet
This section will be updated as sources are added.
Regulatory Documents & Official Trial Registries
No Regulatory Documents & Official Trial Registries Listed Yet
This section will be updated as sources are added.
Anecdotal Reported Patterns — Not Medical Advice
Anecdotal Reported Patterns — Not Medical Advice
Reported dosing patterns are included for educational context only. They are self-reported, unverified, not medical advice, and not instructions for human use. Community-submitted patterns are not yet available in this Phase 1 prototype; this section is a placeholder reserved for moderated, aggregated community data.
Lab Markers to Discuss With a Clinician
Educational topics only — not self-monitoring instructions.
FAQ
Disclaimer
Educational information only. This page summarizes published and official research and does not provide medical advice, a recommendation, or instructions for human use.
Educational use only. This content is provided for informational and research-summary purposes only. It is not medical advice, not a treatment recommendation, not a dosing guide, and not a substitute for care from a licensed medical professional. Nothing here is intended to diagnose, treat, cure, prevent, or mitigate disease. Reported dosing patterns, when shown elsewhere on the site, must be labeled either as Study / Trial Dosing or Anecdotal Reported Patterns — Not Medical Advice. Community reports are self-reported, unverified, and not scientific proof.
Community-reported experiences, once enabled, must be displayed only as moderated, anonymized, or aggregated data. They are anecdotal, self-reported, unverified, and should never be presented as proof of safety, efficacy, or expected results.
Content status: Published. Last updated 2026-08-25.
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