Evidence map›Paper›PMID 14990678›Full record

ArticleThe Journal of physiology2004

Changes in extracellular K+ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K+ current IK1.

Ron Bouchard, Robert B Clark, Alexander E Juhasz, Wayne R Giles

Abstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Article
  2. Article
  3. Effect of inward rectifier potassium 2.1 channel on the osteogenic differentiation of human dental follicle cells and its mechanism.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2022
    Article
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  6. Review
  7. Review
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  9. Article
  10. External KThe Journal of general physiology · 2018
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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

4 authors.

Ron BouchardInstitute of Cardiovascular Sciences, University of Manitoba, St Boniface Research Centre, 351 Taché Avenue, Winnipeg, Manitoba, Canada, R2H 2A6.
Robert B Clark
Alexander E Juhasz
Wayne R Giles

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms underlying the inotropic effect of reductions in [K(+)](o) were studied using recordings of membrane potential, membrane current, cell shortening and [Ca(2+)](i) in single, isolated cardiac myocytes. Three types of mammalian myocytes were chosen, based on differences in the current density and intrinsic voltage dependence of the inwardly rectifying background K(+) current I(K1) in each cell type. Rabbit ventricular myocytes had a relatively large I(K1) with a prominent negative slope conductance whereas rabbit atrial cells expressed much smaller I(K1), with little or no negative slope conductance. I(K1) in rat ventricle was intermediate in both current density and slope conductance. Action potential duration is relatively short in both rabbit atrial and rat ventricular myocytes, and consequently both cell types spend much of the duty cycle at or near the resting membrane potential. Rapid increases or decreases of [K(+)](o) elicited significantly different inotropic effects in rat and rabbit atrial and ventricular myocytes. Voltage-clamp and current-clamp experiments showed that the effects on cell shortening and [Ca(2+)](i) following changes in [K(+)](o) were primarily the result of the effects of alterations in I(K1), which changed resting membrane potential and action potential waveform. This in turn differentially altered the balance of Ca(2+) efflux via the sarcolemmal Na(+)-Ca(2+) exchanger, Ca(2+) influx via voltage-dependant Ca(2+) channels and sarcoplasmic reticulum (SR) Ca(2+) release in each cell type. These results support the hypothesis that the inotropic effect of alterations of [K(+)](o) in the heart is due to significant non-linear changes in the current-voltage relation for I(K1) and the resulting modulation of the resting membrane potential and action potential waveform.

Indexed as

Action PotentialsAnimalsAtrial FunctionCalciumCalcium SignalingCells, CulturedCell SizeHeart AtriaHeart VentriclesIndolesMaleMembrane PotentialsModels, BiologicalMyocardial ContractionMyocytes, CardiacPatch-Clamp TechniquesCalciumindo-1IndolesPotassiumSodium

Identifiers

PMID14990678
PMCPMC1664996

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.