Evidence map›Paper›PMID 17994112›Full record

ArticleBritish journal of pharmacology2008

Effect of K201, a novel antiarrhythmic drug on calcium handling and arrhythmogenic activity of pulmonary vein cardiomyocytes.

Y-J Chen, Y-C Chen, W Wongcharoen, C-I Lin, S-A Chen

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Mechanisms underlying pathological CaPflugers Archiv : European journal of physiology · 2021
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  13. New antiarrhythmic targets to control intracellular calcium handling.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014
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  15. Article
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  17. Novel molecular targets for atrial fibrillation therapy.Nature reviews. Drug discovery · 2012
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Y-J ChenDivision of Cardiovascular Medicine, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan. a9900112@,s15.hinet.net
Y-C Chen
W Wongcharoen
C-I Lin
S-A Chen
National Yang Ming Chiao Tung University · TWWan Fang Hospital · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePulmonary veins are the most important focus for the generation of atrial fibrillation. Abnormal calcium homeostasis with ryanodine receptor dysfunction may underlie the arrhythmogenic activity in pulmonary veins. The preferential ryanodine receptor stabilizer (K201) possesses antiarrhythmic effects through calcium regulation. The purpose of this study was to investigate the effects of K201 on the arrhythmogenic activity and calcium regulation of pulmonary vein cardiomyocytes. EXPERIMENTAL APPROACH: The ionic currents and intracellular calcium were studied in isolated single cardiomyocytes from rabbit pulmonary vein before and after the administration of K201, by the whole-cell patch clamp and indo-1 fluorimetric ratio techniques. KEY

resultsK201 (0.1, 0.3, 1 microM) reduced the firing rates in pulmonary vein cardiomyocytes, decreased the amplitudes of the delayed afterdepolarizations and prolonged the action potential duration. K201 decreased the L-type calcium currents, Na(+)/Ca(2+) exchanger currents, transient inward currents and calcium transients. K201 (1 microM, but not 0.1 microM or 0.3 microM) also reduced the sarcoplasmic reticulum calcium content. Moreover, both the pretreatment and administration of K201 (0.3 microM) decreased the isoprenaline (10 nM)-induced arrhythmogenesis in pulmonary veins. CONCLUSIONS AND IMPLICATIONS: K201 reduced the arrhythmogenic activity of pulmonary vein cardiomyocytes and attenuated the arrhythmogenicity induced by isoprenaline. These findings may reveal the anti-arrhythmic potential of K201.

Indexed as

Action PotentialsAnimalsAnti-Arrhythmia AgentsArrhythmias, CardiacCalciumCalcium Channels, L-TypeDose-Response Relationship, DrugHomeostasisIn Vitro TechniquesIsoproterenolMyocytes, CardiacPulmonary VeinsRabbitsSarcoplasmic ReticulumSodium-Calcium ExchangerThiazepinesAnti-Arrhythmia AgentsCalciumCalcium Channels, L-TypeIsoproterenolK201 compoundSodium-Calcium ExchangerThiazepines

Identifiers

PMID17994112
PMCPMC2267278
OpenAlexW1581310229

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.