Evidence map›Paper›PMID 22198177›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Intracellular Ca2+ release underlies the development of phase 2 in mouse ventricular action potentials.

Marcela Ferreiro, Azadé D Petrosky, Ariel L Escobar

Open access · greenAbstract 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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Regulation of Na/Ca exchange by cytoplasmic protons modifies intracellular calcium dynamics and the cardiac response to ischemia.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  2. Article
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  4. Article
  5. Article
  6. Article
  7. Phase 1 repolarization rate defines CaThe Journal of general physiology · 2019
    Article
  8. Article
  9. Mitochondrial CaJournal of the American Heart Association · 2018
    Article
  10. Article
  11. Article
  12. Chronic atrial ionic remodeling by aldosterone: potentiation of L-type CaPflugers Archiv : European journal of physiology · 2016
    Article
  13. A technical review of optical mapping of intracellular calcium within myocardial tissue.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  14. Article
  15. Article
  16. Chasing cardiac physiology and pathology down the CaMKII cascade.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  17. Article
  18. 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

3 authors at 1 institution in 1 country.

Marcela FerreiroBiological Engineering and Small Scale Technologies Program, School of Engineering, University of California, Merced, CA 95343, USA.
Azadé D Petrosky
Ariel L Escobar
University of California, Merced · US

Funding

Subcellular Origin of T-wave Alternans in the Beating Mouse HeartR01HL084487 · NHLBI · UNIVERSITY OF CALIFORNIA, MERCED · PI ESCOBAR, ARIEL L · 2007 to 2011
$1.9M
NHLBI NIH HHS R01-HL-084487
6 · The paper itself

Abstract

The ventricular action potential (AP) is characterized by a fast depolarizing phase followed by a repolarization that displays a second upstroke known as phase 2. This phase is generally not present in mouse ventricular myocytes. Thus we performed colocalized electrophysiological and optical recordings of APs in Langendorff-perfused mouse hearts founding a noticeable phase 2. Ryanodine as well as nifedipine reduced phase 2. Our hypothesis is that a depolarizing current activated by Ca(2+) released from the sarcoplasmic reticulum (SR) rather than the "electrogenicity" of the L-type Ca(2+) current is crucial in the generation of mouse ventricular phase 2. When Na(+) was partially replaced by Li(+) in the extracellular perfusate or the organ was cooled down, phase 2 was reduced. These results suggest that the Na(+)/Ca(2+) exchanger functioning in the forward mode is driving the depolarizing current that defines phase 2. Phase 2 appears to be an intrinsic characteristic of single isolated myocytes and not an emergent property of the tissue. As in whole heart experiments, ventricular myocytes impaled with microelectrodes displayed a large phase 2 that significantly increases when temperature was raised from 22 to 37°C. We conclude that mouse ventricular APs display a phase 2; however, changes in Ca(2+) dynamics and thermodynamic parameters also diminish phase 2, mostly by impairing the Na(+)/Ca(2+) exchanger. In summary, these results provide important insights about the role of Ca(2+) release in AP ventricular repolarization under physiological and pathological conditions.

Indexed as

Action PotentialsAnimalsCalciumCalcium Channel BlockersCells, CulturedLithiumMiceMice, Inbred C57BLMyocytes, CardiacNifedipineRyanodineSarcoplasmic ReticulumSodium-Calcium ExchangerVentricular FunctionCalciumCalcium Channel BlockersLithiumNifedipineRyanodineSodium-Calcium Exchanger

Identifiers

PMID22198177
PMCPMC3311451
OpenAlexW2116585504

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.