Evidence map›Paper›PMID 21457383›Full record

ArticleJournal of cardiovascular electrophysiology2011

Comparison of the effects of a transient outward potassium channel activator on currents recorded from atrial and ventricular cardiomyocytes.

Kirstine Calloe, Eyal Nof, Thomas Jespersen, José M Di Diego, Natalie Chlus, Søren-Peter Olesen, Charles Antzelevitch, Jonathan M Cordeiro

Abstract readComparative Study
In one paragraph

Article in Journal of cardiovascular electrophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Inducing IJournal of molecular and cellular cardiology · 2022
    Article
  2. Review
  3. Article
  4. Auxiliary subunits control biophysical properties and response to compound NS5806 of the Kv4 potassium channel complex.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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  11. Review
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  14. Tissue-specific effects of acetylcholine in the canine heart.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  15. Article
  16. Article
  17. Article
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

8 authors.

Kirstine CalloeDanish National Research Foundation Center for Cardiac Arrhythmias, University of Copenhagen, Copenhagen, Denmark.
Eyal Nof
Thomas Jespersen
José M Di Diego
Natalie Chlus
Søren-Peter Olesen
Charles Antzelevitch
Jonathan M Cordeiro

Funding

ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIASR01HL047678 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI ANTZELEVITCH, CHARLES · 1993 to 2014
$5.7M
ELECTRICAL HETEROGENEITY AND CARDIAC ARRHYTHMIASR55HL047678 · NHLBI · MASONIC MEDICAL RESEARCH LABORATORY, INC · PI ANTZELEVITCH, CHARLES · 1992 to 1992
–
NHLBI NIH HHS HL47678NHLBI NIH HHS R01 HL047678
6 · The paper itself

Abstract

introductionNS5806 activates the transient outward potassium current (I(to) ) in canine ventricular cells. We compared the effects of NS5806 on canine atrial versus ventricular tissues and myocytes. METHODS AND

resultsNS5806 (10 μM) was evaluated in arterially perfused canine right atrial and right ventricular wedge preparations. In ventricular wedges NS5806 (10 μM) accentuated phase 1 in epicardium (Epi), with little effect in endocardium (Endo), resulting in augmented J-waves on the ECG. In contrast, application of NS5806 (10 μM) to atrial preparations had no effect on phase 1 repolarization but significantly decreased upstroke velocity (dV/dt) and depressed excitability, consistent with sodium channel block. Current and voltage-clamp recordings were made in the absence and presence of NS5806 in (10 μM) enzymatically dissociated atrial and ventricular myocytes. In ventricular myocytes, NS5806 increased I(to) magnitude by 80% and 16% in Epi and Endo, respectively (at +40 mV). In atrial myocytes, NS5806 increased peak I(to) by 25% and had no effect on the sustained current, I(Kur) . Under control conditions, I(Na) density in atrial myocytes was nearly double that in ventricular myocytes. NS5806 caused a shift in steady-state mid-inactivation (V(1/2)) from -73.9 ± 0.27 to -77.3 ± 0.21 mV in ventricular and from -82.6 ± 0.12 to -85.1 ± 0.11 mV in atrial cells, resulting in reduction of I(Na) in both cell types. Expression of mRNA encoding putative I(Na) and I(to) channel subunits was evaluated by qPCR.

conclusionNS5806 produces a prominent augmentation of I(to) with little effect on I(Na) in the ventricles, but a potent inhibition of I(Na) with little augmentation of I(to) in atria.

Indexed as

Action PotentialsAnimalsDogsFemaleHeart AtriaHeart VentriclesMaleMyocytes, CardiacPhenylurea CompoundsPotassium ChannelsTetrazoles1-(3,5-bis-trifluoromethylphenyl)-3-(2,4-dibromo-6-(1H-tetrazol-5-yl)phenyl)ureaPhenylurea CompoundsPotassium ChannelsTetrazoles

Identifiers

PMID21457383
PMCPMC3136585

What OpenQuestion holds

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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.