Evidence map›Paper›PMID 27496871›Full record

ArticleCardiovascular research2016

C-type natriuretic peptide and natriuretic peptide receptor B signalling inhibits cardiac sympathetic neurotransmission and autonomic function.

Jens Buttgereit, Julia Shanks, Dan Li, Guoliang Hao, Arvinder Athwal, Thomas H Langenickel, Hannah Wright, Andrey C da Costa Goncalves, Jan Monti, Ralph Plehm and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 39 citations in OpenAlex.

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  12. C-type natriuretic peptide is a pivotal regulator of metabolic homeostasis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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  18. Imaging of PDE2- and PDE3-Mediated cGMP-to-cAMP Cross-Talk in Cardiomyocytes.Journal of cardiovascular development and disease · 2018
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 3 countries.

Jens ButtgereitExperimental and Clinical Research Center (ECRC), a joint institution of the Max Delbrück Center for Molecular Medicine (MDC) and the Charité Medical Faculty, Berlin, Germany.
Julia ShanksBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Dan LiBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Guoliang HaoBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Arvinder AthwalBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Thomas H LangenickelTranslational Medicine, Clinical Pharmacology and Profiling, Novartis Pharma AG, Basel, Switzerland.
Hannah WrightBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Andrey C da Costa GoncalvesLeibniz Institute for Molecular Pharmacology (FMP), Campus Berlin-Buch, Berlin, Germany.
Jan MontiHelios Clinic Bad Saarow, Pieskower Strasse 33, Bad Saarow, Germany.
Ralph PlehmMax Delbrück Center for Molecular Medicine (MDC), Campus Berlin-Buch, Robert-Rössle-Strasse 10, 13092 Berlin, Germany.
Elena PopovaMax Delbrück Center for Molecular Medicine (MDC), Campus Berlin-Buch, Robert-Rössle-Strasse 10, 13092 Berlin, Germany.
Fatimunnisa QadriExperimental and Clinical Research Center (ECRC), a joint institution of the Max Delbrück Center for Molecular Medicine (MDC) and the Charité Medical Faculty, Berlin, Germany.
Irina LapidusMax Delbrück Center for Molecular Medicine (MDC), Campus Berlin-Buch, Robert-Rössle-Strasse 10, 13092 Berlin, Germany.
Brent RyanBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Cemil ÖzcelikExperimental and Clinical Research Center (ECRC), a joint institution of the Max Delbrück Center for Molecular Medicine (MDC) and the Charité Medical Faculty, Berlin, Germany.
David J PatersonBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK.
Michael BaderMax Delbrück Center for Molecular Medicine (MDC), Campus Berlin-Buch, Robert-Rössle-Strasse 10, 13092 Berlin, Germany neilherring@doctors.org.uk mbader@mdc-berlin.de.
Neil HerringBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Parks Road, Oxford OX13PT, UK neilherring@doctors.org.uk mbader@mdc-berlin.de.
University of Oxford · GBMax Delbrück Center · DECharité - Universitätsmedizin Berlin · DEHelios Hospital Bad Saarow · DELeibniz Association · DE

Funding

British Heart Foundation FS/15/8/31155British Heart Foundation PG/12/87/29943British Heart Foundation PG/14/13/30680
6 · The paper itself

Abstract

aimsB-type natriuretic peptide (BNP)-natriuretic peptide receptor A (NPR-A) receptor signalling inhibits cardiac sympathetic neurotransmission, although C-type natriuretic peptide (CNP) is the predominant neuropeptide of the nervous system with expression in the heart and vasculature. We hypothesized that CNP acts similarly to BNP, and that transgenic rats (TGRs) with neuron-specific overexpression of a dominant negative NPR-B receptor would develop heightened sympathetic drive. METHODS AND

resultsMean arterial pressure and heart rate (HR) were significantly (P < 0.05) elevated in freely moving TGRs (n = 9) compared with Sprague Dawley (SD) controls (n = 10). TGR had impaired left ventricular systolic function and spectral analysis of HR variability suggested a shift towards sympathoexcitation. Immunohistochemistry demonstrated co-staining of NPR-B with tyrosine hydroxylase in stellate ganglia neurons. In SD rats, CNP (250 nM, n = 8) significantly reduced the tachycardia during right stellate ganglion stimulation (1-7 Hz) in vitro whereas the response to bath-applied norepinephrine (NE, 1 μM, n = 6) remained intact. CNP (250 nM, n = 8) significantly reduced the release of

conclusionC-type natriuretic peptide reduces cardiac sympathetic neurotransmission via a reduction in neuronal calcium signalling and NE release through the NPR-B receptor. Situations impairing CNP-NPR-B signalling lead to hypertension, tachycardia, and impaired left ventricular systolic function secondary to sympatho-excitation.

Indexed as

Synaptic TransmissionAnimalsArterial PressureAtrial Natriuretic Factor Receptor BCalcium SignalingGenetic Predisposition to DiseaseHeartHeart RateHypertensionNatriuretic Peptide, C-TypeNorepinephrinePhenotypeRats, Sprague-DawleyRats, TransgenicReceptors, Atrial Natriuretic FactorStellate GanglionAtrial Natriuretic Factor Receptor BNatriuretic Peptide, C-TypeNorepinephrineReceptors, Atrial Natriuretic FactorTyrosine 3-MonooxygenaseCalciumHypertensionNatriuretic peptidesNorepinephrineSympathetic

Identifiers

PMID27496871
PMCPMC5157132
OpenAlexW2502906121

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.