ArticleActa pharmacologica Sinica2009
Inhibitory effects of tetrandrine on the Na(+) channel of human atrial fibrillation myocardium.
Article in Acta pharmacologica Sinica, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Tetrandrine ameliorated atherosclerosis in vitamin D3/high cholesterol diet-challenged rats via modulation of miR-34a and Wnt5a/Ror2/ABCA1/NF-kB trajectory.Scientific reports · 2024Article
- Organization of atrial fibrillation using a pure sodium channel blocker: Implications of rotor ablation therapy.Journal of arrhythmia · 2023Article
- Research Progress on Natural Products' Therapeutic Effects on Atrial Fibrillation by Regulating Ion Channels.Cardiovascular therapeutics · 2022Review
- A review on plants and herbal components with antiarrhythmic activities and their interaction with current cardiac drugs.Journal of traditional and complementary medicine · 2020Review
- A critical review: traditional uses, phytochemistry, pharmacology and toxicology ofPhytochemistry reviews : proceedings of the Phytochemical Society of Europe · 2020Review
- In Vitro Study of the Metabolic Characteristics of Eight Isoquinoline Alkaloids from Natural Plants in Rat Gut Microbiota.Molecules (Basel, Switzerland) · 2017Article
- Azelnidipine is a calcium blocker that attenuates liver fibrosis and may increase antioxidant defence.British journal of pharmacology · 2012Article
- Irbesartan prevents sodium channel remodeling in a canine model of atrial fibrillation.Journal of the renin-angiotensin-aldosterone system : JRAASArticle
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTetrandrine (Tet) is a Ca(2+) channel blocker and has antiarrhythmic effects. Less information exists with regard to the mechanisms underlying its antiarrhythmic action other than blocking Ca(2+) channels. In this study, the effects of Tet on the Na(+) current (I(Na)) in the atrial myocardium of patients in atrial fibrillation (AF) and sinus rhythm (SR) were investigated, and the characteristics of the Na(+) current were synchronously compared between the AF and SR patients.
methodsNa(+) currents were recorded using the whole-cell patch clamp technique in single atrial myocyte of the AF and the normal SR groups. The effects of Tet (40-120 micromol/L) on the Na(+) current in the two groups were then observed.
resultsTet (60-120 micromol/L) decreased I(Na) density in a concentration-dependent manner and made the voltage-dependent activation curve shift to more positive voltages in the SR and AF groups. After exposure to Tet, the voltage-dependent inactivation curve of I(Na) was shifted to more negative voltages in the two groups. Tet delayed the time-dependent recovery of I(Na) in a concentration dependent manner in both AF and SR cells; however, there were no differences in the effects of Tet on I(Na) density and properties in the two groups. The I(Na) density of AF patients did not differ from that of the SR patients.
conclusionTet can block sodium channels with slow recovery kinetics, which may explain the mechanisms underlying the antiarrhythmic action of Tet. The decreased conduction velocity (CV) in AF patients is not caused by the Na(+) current.
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