Evidence map›Paper›PMID 26203906›Full record

ArticlePloS one2015

Norepinephrine-Induced Adrenergic Activation Strikingly Increased the Atrial Fibrillation Duration through β1- and α1-Adrenergic Receptor-Mediated Signaling in Mice.

Kenji Suita, Takayuki Fujita, Nozomi Hasegawa, Wenqian Cai, Huiling Jin, Yuko Hidaka, Rajesh Prajapati, Masanari Umemura, Utako Yokoyama, Motohiko Sato and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  5. A novel technique for vein of Marshall blood sampling and its application in assessing atrial remodeling in atrial fibrillation.Clinical research in cardiology : official journal of the German Cardiac Society · 2025
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  14. Adrenoceptor sub-type involvement in CaPflugers Archiv : European journal of physiology · 2022
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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

12 authors at 3 institutions in 1 country.

Kenji SuitaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Takayuki FujitaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Nozomi HasegawaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Wenqian CaiCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Huiling JinCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yuko HidakaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Rajesh PrajapatiCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Masanari UmemuraCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Utako YokoyamaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Motohiko SatoCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan; Department of Physiology, Aichi Medical University School of Medicine, Aichi, Japan.
Satoshi OkumuraCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan; Department of Physiology, Tsurumi University School of Dental Medicine, Yokohama, Japan.
Yoshihiro IshikawaCardiovascular Research Institute, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yokohama City University · JPCardiovascular Institute Hospital · JPAichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtrial fibrillation (AF) is the most common arrhythmias among old people. It causes serious long-term health problems affecting the quality of life. It has been suggested that the autonomic nervous system is involved in the onset and maintenance of AF in human. However, investigation of its pathogenesis and potential treatment has been hampered by the lack of suitable AF models in experimental animals.

objectivesOur aim was to establish a long-lasting AF model in mice. We also investigated the role of adrenergic receptor (AR) subtypes, which may be involved in the onset and duration of AF. METHODS AND

resultsTrans-esophageal atrial burst pacing in mice could induce AF, as previously shown, but with only a short duration (29.0 ± 8.1 sec). We found that adrenergic activation by intraperitoneal norepinephrine (NE) injection strikingly increased the AF duration. It increased the duration to more than 10 minutes, i.e., by more than 20-fold (656.2 ± 104.8 sec; P<0.001). In this model, a prior injection of a specific β1-AR blocker metoprolol and an α1-AR blocker prazosin both significantly attenuated NE-induced elongation of AF. To further explore the mechanisms underlying these receptors' effects on AF, we assessed the SR Ca(2+) leak, a major trigger of AF, and consequent spontaneous SR Ca(2+) release (SCR) in atrial myocytes. Consistent with the results of our in-vivo experiments, both metoprolol and prazosin significantly inhibited the NE-induced SR Ca(2+) leak and SCR. These findings suggest that both β1-AR and α1-AR may play important roles in the development of AF.

conclusionsWe have established a long-lasting AF model in mice induced by adrenergic activation, which will be valuable in future AF study using experimental animals, such as transgenic mice. We also revealed the important role of β1- and α1-AR-mediated signaling in the development of AF through in-vivo and in-vitro experiments.

Indexed as

Disease Models, AnimalAdrenergic alpha-AntagonistsAdrenergic beta-AntagonistsAnimalsAtrial FibrillationCalcium SignalingCells, CulturedHeart Conduction SystemInjections, IntraperitonealMaleMetoprololMiceMice, Inbred C57BLMyocytes, CardiacNorepinephrinePrazosinAdrenergic alpha-AntagonistsAdrenergic beta-AntagonistsMetoprololNorepinephrinePrazosinReceptors, Adrenergic, alpha-1Receptors, Adrenergic, beta-1

Identifiers

PMID26203906
PMCPMC4512675
OpenAlexW1544396097

What OpenQuestion holds

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LicenceCC BY
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.