Evidence map›Paper›PMID 22904161›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Regulation of cardiac alternans by β-adrenergic signaling pathways.

Stela M Florea, Lothar A Blatter

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. 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
1.7field-weighted citation impact, top 14% of its field
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, 37 citations in OpenAlex.

  1. Article
  2. Review
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  7. Mitochondrial calcium uniporter complex activation protects against calcium alternans in atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  8. Article
  9. Article
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  12. Article
  13. CaAmerican journal of physiology. Heart and circulatory physiology · 2017
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cardiac alternans and intracellular calcium cycling.Clinical and experimental pharmacology & physiology · 2014
    Review
  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 at 1 institution in 1 country.

Stela M FloreaDepartment of Molecular Biophysics and Physiology, Rush University Medical Center, Chicago, Illinois 60612, USA.
Lothar A Blatter
Rush University Medical Center · US

Funding

Program AdministrationP01HL080101 · NHLBI · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BERS, DONALD M · 2006 to 2015
$23.4M
E/C COUPLING AND CALCIUM REGULATION IN ATRIAL MYOCYTESR01HL062231 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI BLATTER, LOTHAR A · 1999 to 2012
$4.4M
MItochondrial Dysfunction in Cardiac Hypertrophy and FailureR01HL101235 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BERS, DONALD M, BLATTER, LOTHAR A · 2010 to 2013
$2.8M
NHLBI NIH HHS HL-101235NHLBI NIH HHS HL-62231NHLBI NIH HHS HL-80101
6 · The paper itself

Abstract

In cat atrial myocytes, β-adrenergic receptor (β-AR) stimulation exerts profound effects on excitation-contraction coupling and cellular Ca(2+) cycling that are mediated by β(1)- and β(2)-AR subtypes coupled to G proteins (G(s) and G(i)). In this study, we determined the effects of β-AR stimulation on pacing-induced Ca(2+) alternans. Ca(2+) alternans was recorded from single cat atrial myocytes with the fluorescent Ca(2+) indicator indo-1. Stable Ca(2+) alternans occurred at an average pacing frequency of 1.7 Hz at room temperature with a mean alternans ratio of 0.43. Nonselective β-AR stimulation as well as selective stimulation of β(1)/G(s), β(2)/G(s) + G(i), and β(2)/G(s) coupled pathways all abolished pacing-induced Ca(2+) alternans. β(1)-AR stimulation abolished alternans through stimulation of PKA and Ca(2+)/calmodulin-dependent protein kinase II, whereas β(2)-AR stimulation exclusively involved PKA and was mediated via G(s), whereas a known second pathway in cat atrial myocytes acting through G(i) and nitric oxide production was not involved in alternans regulation. Inhibition of various mitochondrial functions (dissipation of the mitochondrial membrane potential or inhibition of mitochondrial F(1)/F(0)-ATP synthase, mitochondrial Ca(2+) uptake via the mitochondrial Ca(2+) uniporter, and Ca(2+) extrusion via mitochondrial Na(+)/Ca(2+) exchange) enhanced Ca(2+) alternans; however, β-AR stimulation still abrogated alternans, provided that sufficient cellular ATP was available. Selective inhibition of mitochondrial or glycolytic ATP production did not prevent β-AR stimulation from abolishing Ca(2+) alternans. However, when both ATP sources were depleted, β-AR stimulation failed to decrease Ca(2+) alternans. These results indicate that in atrial myocytes, β-AR stimulation protects against pacing-induced alternans by acting through parallel and complementary signaling pathways.

Indexed as

Adenosine TriphosphateAnimalsArrhythmias, CardiacCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium ChannelsCalmodulinCatsCells, CulturedCyclic AMP-Dependent Protein KinasesEnergy MetabolismHeart AtriaHeart Conduction SystemMitochondriaMyocardial ContractionMyocytes, CardiacAdenosine TriphosphateCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium ChannelsCalmodulinCyclic AMP-Dependent Protein KinasesReceptors, Adrenergic, beta-1Receptors, Adrenergic, beta-2

Identifiers

PMID22904161
PMCPMC3469647
OpenAlexW2141646835

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.