Evidence map›Paper›PMID 11410639›Full record

ArticleThe Journal of physiology2001

Modulation of the Ca(2+)-induced Ca(2+) release cascade by beta-adrenergic stimulation in rat ventricular myocytes.

S Viatchenko-Karpinski, S Györke

Abstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

  1. Autonomic control of ventricular function in health and disease: current state of the art.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The nervous heart.Progress in biophysics and molecular biology · 2016
    Review
  8. Article
  9. Sex differences in mechanisms of cardiac excitation-contraction coupling.Pflugers Archiv : European journal of physiology · 2013
    Review
  10. Article
  11. Article
  12. Article
  13. Ryanodine receptor/calcium release channel PKA phosphorylation: a critical mediator of heart failure progression.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  14. Article
  15. Article
  16. Article
  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

2 authors.

S Viatchenko-KarpinskiDepartment of Physiology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.
S Györke

Funding

ADAPTATION--CONTROL MECHANISM OF CA2 RELEASE IN HEARTR29HL052620 · NHLBI · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI GYORKE, SANDOR · 1995 to 1998
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NHLBI NIH HHS HL 03739NHLBI NIH HHS HL 52620
6 · The paper itself

Abstract

1. To define the sub-cellular mechanisms of modulation of cardiac excitation-contraction (E-C) coupling by the beta-adrenergic pathway, we carried out confocal Ca(2+) imaging in conjunction with recordings of inward Ca(2+) current in fluo-3-loaded patch-clamped rat ventricular myocytes. 2. Isoproterenol (isoprenaline; ISO) increased the amplitude of the inward Ca(2+) current and the globally measured intracellular Ca(2+) transients. The gain of calcium-induced calcium release (CICR) was increased at all membrane potentials but especially at positive membrane potentials (> +30 mV). ISO dramatically broadened the bell-shaped voltage dependence of intracellular Ca(2+) transients by shifting the descending portion of the curve to very high membrane potentials. 3. The number of local release events (solitary sparks and conglomerates of overlapping sparks) induced by depolarizing steps to +30 mV was increased significantly by ISO. This potentiation of events was due to increased trigger calcium current (I(Ca)) as well the enhanced ability of I(Ca) to induce release. The amplitude and duration of solitary sparks were increased in the presence of ISO. In addition, ISO dramatically increased the proportion and the size ('mass') of clustered events. 4. Exclusion of Na(+) from the intra- and extracellular solutions prevented ISO from enhancing the ability of I(Ca) to trigger sparks. 5. We conclude that beta-adrenergic stimulation enhances the gain of the CICR cascade by increasing the fidelity of dihydropyridine receptor (DHPR)--ryanodine receptor (RyR) coupling and by promoting cross-activation of RyRs in neighbouring release sites. Reverse Na(+)--Ca(2+) exchange (NCX) appears to play a role in the beta-adrenergic enhancement of CICR by effectively contributing to the Ca(2+) trigger.

Indexed as

Adrenergic beta-AgonistsAnimalsCalciumElectric ConductivityElectrophysiologyExtracellular SpaceHeart VentriclesIntracellular MembranesIsoproterenolMembrane PotentialsMyocardiumPatch-Clamp TechniquesRatsRats, Sprague-DawleyReceptors, Adrenergic, betaSarcoplasmic ReticulumAdrenergic beta-AgonistsCalciumIsoproterenolReceptors, Adrenergic, betaSodium

Identifiers

PMID11410639
PMCPMC2278674

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.