Evidence map›Paper›PMID 10226162›Full record

ArticleThe Journal of physiology1999

Relationship between K+ channel down-regulation and [Ca2+]i in rat ventricular myocytes following myocardial infarction.

R Kaprielian, A D Wickenden, Z Kassiri, T G Parker, P P Liu, P H Backx

Abstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing 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

48 citing papers in PubMed.

  1. High-density isochronal repolarization mapping and re-entry vulnerability estimation for scar-related ventricular tachycardia ablation: mechanistic basis, clinical application, and challenges.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024
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  7. Impact of intracellular hemin on N-type inactivation of voltage-gated KPflugers Archiv : European journal of physiology · 2020
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  11. Notch signaling modulates the electrical behavior of cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2018
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  20. Hyperoxia-induced hypertrophy and ion channel remodeling in left ventricle.American journal of physiology. Heart and circulatory physiology · 2013
    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

6 authors.

R KaprielianDepartment of Medicine, University of Toronto, Toronto, Ontario, Canada M5G 2C4.
A D Wickenden
Z Kassiri
T G Parker
P P Liu
P H Backx

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Cardiac hypertrophy and prolongation of the cardiac action potential are hallmark features of heart disease. We examined the molecular mechanisms and the functional consequences of this action potential prolongation on calcium handling in right ventricular myocytes obtained from rats 8 weeks following ligation of the left anterior descending coronary artery (post-myocardial infarction (MI) myocytes). 2. Compared with myocytes from sham-operated rats (sham myocytes), post-MI myocytes showed significant reductions in transient outward K+ current (Ito) density (sham 19.7 +/- 1.1 pA pF-1 versus post-MI 11.0 +/- 1.3 pA pF-1; means +/- s.e.m.), inward rectifier K+ current density (sham -13.7 +/- 0.6 pA pF-1 versus post-MI -10.3 +/- 0.9 pA pF-1) and resting membrane potential (sham -84.4 +/- 1.3 mV versus post-MI -74.1 +/- 2.6 mV). Depressed Ito amplitude correlated with significant reductions in Kv4.2 and Kv4.3 mRNA and Kv4.2 protein levels. Kv1.4 mRNA and protein levels were increased and coincided with the appearance of a slow component of recovery from inactivation for Ito. 3. In current-clamp recordings, post-MI myocytes showed a significant increase in [Ca2+]i transient amplitude compared with sham myocytes. Using voltage-clamp depolarizations, no intrinsic differences in Ca2+ handling by the sarcoplasmic reticulum or in L-type Ca2+ channel density (ICa,L) were detected between the groups. 4. Stimulation of post-MI myocytes with an action potential derived from a sham myocyte reduced the [Ca2+] transient amplitude to the sham level and vice versa. 5. The net Ca2+ influx per beat via ICa,L was increased about 2-fold in myocytes stimulated with post-MI action potentials compared with sham action potentials. 6. Our findings demonstrate that reductions in K+ channel expression in post-MI myocytes prolong action potential duration resulting in elevated Ca2+ influx and [Ca2+]i transients.

Indexed as

Action PotentialsAnimalsCalciumCalcium ChannelsDisease Models, AnimalDown-RegulationHeart VentriclesIntracellular FluidIon TransportMaleMembrane PotentialsMyocardial InfarctionMyocardiumPatch-Clamp TechniquesPotassium ChannelsRatsCalciumCalcium ChannelsPotassium ChannelsRNA, Messenger

Identifiers

PMID10226162
PMCPMC2269317

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.