Evidence map›Paper›PMID 27528004›Full record

ArticlePhysiological reports2016

The role of GαO-mediated signaling in the rostral ventrolateral medulla oblongata in cardiovascular reflexes and control of cardiac ventricular excitability.

Richard Ang, Joel Abramowitz, Lutz Birnbaumer, Alexander V Gourine, Andrew Tinker

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. GPCR-dependent biasing of GIRK channel signaling dynamics by RGS6 in mouse sinoatrial nodal cells.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  3. Article
  4. Article
  5. 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

5 authors at 3 institutions in 2 countries.

Richard AngWilliam Harvey Heart Centre, Barts & The London School of Medicine and Dentistry, London, UK Department of Neuroscience, Physiology and Pharmacology, University College London, London, UK.
Joel AbramowitzDivision of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.
Lutz BirnbaumerDivision of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina.
Alexander V GourineWilliam Harvey Heart Centre, Barts & The London School of Medicine and Dentistry, London, UK.
Andrew TinkerDepartment of Neuroscience, Physiology and Pharmacology, University College London, London, UK a.tinker@qmul.ac.uk.
National Institute of Environmental Health Sciences · USUniversity College London · GBWilliam Harvey Research Institute · GB

Funding

British Heart Foundation RG/14/4/30736Medical Research Council G0901948Wellcome Trust 095064
6 · The paper itself

Abstract

The heart is controlled by the sympathetic and parasympathetic limbs of the autonomic nervous system with inhibitory signaling mechanisms recruited in both limbs. The aim of this study was to determine the role of inhibitory heterotrimeric G proteins in the central nervous mechanisms underlying autonomic control of the heart and its potential role in arrhythmogenesis. Mice with conditional deletion of the inhibitory heterotrimeric G protein GαO in the presympathetic area of the rostral ventral lateral medulla (RVLM) were generated to determine the role of GαO-mediated signalling in autonomic control and electrophysiological properties of the heart. GαO deletion within the RVLM was not associated with changes in heart rate (HR) or the arterial blood pressure at rest (home cage, normal behavior). However, exposure to stressful conditions (novel environment, hypoxia, or hypercapnia) in these mice was associated with abnormal HR responses and an increased baroreflex gain when assessed under urethane anesthesia. This was associated with shortening of the ventricular effective refractory period. This phenotype was reversed by systemic beta-adrenoceptor blockade, suggesting that GαO depletion in the RVLM increases central sympathetic drive. The data obtained support the hypothesis that GαO-mediated signaling within the presympathetic circuits of the RVLM contributes to the autonomic control of the heart. GαO deficiency in the RVLM has a significant impact on cardiovascular responses to stress, cardiovascular reflexes and electrical properties of the heart.

Indexed as

AnimalsAutonomic Nervous SystemBlood PressureGTP-Binding Protein alpha Subunits, Gi-GoHeartHeart RateHemodynamicsHypercapniaHypoxiaMedulla OblongataMiceMice, TransgenicRespirationSignal TransductionVentricular FunctionGNAO1 protein, mouseGTP-Binding Protein alpha Subunits, Gi-GoAutonomic nervous systemblood pressurecardiac excitabilityG proteinsrostral ventral lateral medulla

Identifiers

PMID27528004
PMCPMC4985541
OpenAlexW2513700252

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.