ArticleThe Journal of membrane biology2005
State-dependent block of human cardiac hNav1.5 sodium channels by propafenone.
Article in The Journal of membrane biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Late IMedicinal research reviews · 2026Review
- Computational Modeling for Antiarrhythmic Drugs for Atrial Fibrillation According to Genotype.Frontiers in physiology · 2021Article
- Tetrodotoxin-Sensitive Neuronal-Type NaJournal of the American Heart Association · 2020Article
- "Pill-in-the-Pocket" Treatment of Propafenone Unmasks ECG Brugada Pattern in an Atrial Fibrillation Patient With a Common SCN5A R1193Q Polymorphism.Frontiers in physiology · 2019Article
- Article
- Pharmacology of the NaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Reporting sodium channel activity using calcium flux: pharmacological promiscuity of cardiac Nav1.5.Molecular pharmacology · 2015Article
- The role of late I Na in development of cardiac arrhythmias.Handbook of experimental pharmacology · 2014Review
- Mechanisms of atrial-selective block of Na⁺ channels by ranolazine: II. Insights from a mathematical model.American journal of physiology. Heart and circulatory physiology · 2011Article
- State- and use-dependent block of muscle Nav1.4 and neuronal Nav1.7 voltage-gated Na+ channel isoforms by ranolazine.Molecular pharmacology · 2008Article
- Persistent human cardiac Na+ currents in stably transfected mammalian cells: Robust expression and distinct open-channel selectivity among Class 1 antiarrhythmics.Channels (Austin, Tex.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
State-dependent blockade of human cardiac hNav1.5 sodium channels by propafenone was studied using whole-cell patch clamp techniques. Both a direct investigation using cells with inactivation-deficient sodium channels and an algorithmic approach used on cells with wild-type channels revealed a rapid binding of propafenone to the open state. This occurs approximately 4000 and 700 times faster than the binding to the resting and inactivated state, respectively. An established mathematical "gating" model was modified to represent the experimental data.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.