Component

Human cardiac sodium channel Nav1.5 / SCN5A

Species, preparation, dose and limitations are retained on linked claims.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

  1. Eugenol concentration-dependently inhibited human Nav1.5, favored the inactivated state, slowed recovery, and attenuated late sodium current.

    Eugenol → Human cardiac Nav1.5 sodium current source_derived_draftungraded
    Experimental context and source evidence
    dose
    Eugenol concentration-response; ouabain arrhythmia model
    duration
    Acute
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    HEK cells expressing human Nav1.5; isolated guinea-pig atria
    limitations
    Channel inhibition can alter cardiac excitability; isolated atrial antiarrhythmic effects are not a human treatment result.
    nutrient_topic
    Eugenol chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Eugenol
    organism
    HEK cells expressing human Nav1.5; isolated guinea-pig atria
    plain_language
    Eugenol concentration-dependently inhibited human Nav1.5, favored the inactivated state, slowed recovery, and attenuated late sodium current.
    primary_references
    Eugenol interacts with cardiac sodium channel and reduces heart excitability and arrhythmias. (2021). https://pubmed.ncbi.nlm.nih.gov/34217764/ DOI: 10.1016/j.lfs.2021.119761
    route
    In vitro and ex vivo
    tissue
    Cardiac sodium current and ex-vivo rhythm disturbance

    Eugenol: mechanism of action and interactions (2026-09-20) · lines 55–64

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · HEK cells expressing human Nav1.5; isolated guinea-pig atria · source_derived_draft · unverified_draft

    ## eugenol-nav15 Eugenol concentration-dependently inhibited human Nav1.5, favored the inactivated state, slowed recovery, and attenuated late sodium current. Model/species: HEK cells expressing human Nav1.5; isolated guinea-pig atria Tissue/system: Cardiac sodium current and ex-vivo rhythm disturbance Exposure: Eugenol concentration-response; ouabain arrhythmia model Route: In vitro and ex vivo Duration: Acute Limits: Channel inhibition can alter cardiac excitability; isolated atrial antiarrhythmic effects are not a human treatment result. Primary reference: Eugenol interacts with cardiac sodium channel and reduces heart excitability and arrhythmias. (2021). https://pubmed.ncbi.nlm.nih.gov/34217764/ DOI: 10.1016/j.lfs.2021.119761 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards