Evidence map›Paper›PMID 24535581›Full record

ArticlePflugers Archiv : European journal of physiology2014

Beta-adrenergic stimulation reverses the I Kr-I Ks dominant pattern during cardiac action potential.

Tamas Banyasz, Zhong Jian, Balazs Horvath, Shaden Khabbaz, Leighton T Izu, Ye Chen-Izu

Abstract read
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing 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

36 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Predicting the Damaging Potential of UncharacterizedInternational journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. International journal of molecular sciences · 2024
    Article
  9. Article
  10. Article
  11. Article
  12. Pro-arrhythmic effects of gain-of-function potassium channel mutations in the short QT syndrome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023
    Review
  13. IBiomedicines · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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.

Tamas BanyaszDepartment of Pharmacology, University of California, 2221 Tupper Hall, 451 Health Science Drive, Davis, CA, 95616, USA.
Zhong Jian
Balazs Horvath
Shaden Khabbaz
Leighton T Izu
Ye Chen-Izu

Funding

Sarcomere Length Shortening and the Destabilization of the Ca2+ Control System inR01HL090880 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI IZU, LEIGHTON T. · 2009 to 2012
$1.5M
CaMKII Inhibition as a New Therapeutic Strategy for Treating Hypertension-inducedR03AG031944 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CHEN-IZU, YE · 2009 to 2010
$125k
NHLBI NIH HHS HL90880NHLBI NIH HHS R01 HL090880NIA NIH HHS AG031944NIA NIH HHS R03 AG031944
6 · The paper itself

Abstract

β-Adrenergic stimulation differentially modulates different K(+) channels and thus fine-tunes cardiac action potential (AP) repolarization. However, it remains unclear how the proportion of I Ks, I Kr, and I K1 currents in the same cell would be altered by β-adrenergic stimulation, which would change the relative contribution of individual K(+) current to the total repolarization reserve. In this study, we used an innovative AP-clamp sequential dissection technique to directly record the dynamic I Ks, I Kr, and I K1 currents during the AP in guinea pig ventricular myocytes under physiologically relevant conditions. Our data provide quantitative measures of the magnitude and time course of I Ks, I Kr, and I K1 currents in the same cell under its own steady-state AP, in a physiological milieu, and with preserved Ca(2+) homeostasis. We found that isoproterenol treatment significantly enhanced I Ks, moderately increased I K1, but slightly decreased I Kr in a dose-dependent manner. The dominance pattern of the K(+) currents was I Kr > I K1 > I Ks at the control condition, but reversed to I Kr < I K1 < I Ks following β-adrenergic stimulation. We systematically determined the changes in the relative contribution of I Ks, I Kr, and I K1 to cardiac repolarization during AP at different adrenergic states. In conclusion, the β-adrenergic stimulation fine-tunes the cardiac AP morphology by shifting the power of different K(+) currents in a dose-dependent manner. This knowledge is important for designing antiarrhythmic drug strategies to treat hearts exposed to various sympathetic tones.

Indexed as

Action PotentialsAdrenergic AgentsAnimalsAnti-Arrhythmia AgentsCalciumGuinea PigsHeartHeart VentriclesIsoproterenolMaleMyocardiumMyocytes, CardiacPatch-Clamp TechniquesPotassiumPotassium ChannelsVentricular FunctionAdrenergic AgentsAnti-Arrhythmia AgentsCalciumIsoproterenolPotassiumPotassium Channels

Identifiers

PMID24535581
PMCPMC4138296

What OpenQuestion holds

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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.