Evidence map›Paper›PMID 29203815›Full record

ArticleScientific reports2017

Role of ventral medullary catecholaminergic neurons for respiratory modulation of sympathetic outflow in rats.

Davi J A Moraes, Leni G H Bonagamba, Melina P da Silva, Julian F R Paton, Benedito H Machado

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Neuronal Networks in Hypertension: Recent Advances.Hypertension (Dallas, Tex. : 1979) · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Review
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 3 countries.

Davi J A MoraesSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil. davimoraes@fmrp.usp.br.ORCID 0000-0001-6132-0217
Leni G H BonagambaSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.
Melina P da SilvaSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.
Julian F R PatonSchool of Physiology, Pharmacology and Neuroscience, Biomedical Sciences, University of Bristol, Bristol, UK.
Benedito H MachadoSchool of Medicine of Ribeirão Preto, Department of Physiology, University of São Paulo, Ribeirão Preto, SP, Brazil.
Universidade de São Paulo · BRUniversidade de Ribeirão Preto · BRUniversity of Auckland · NZ

Funding

British Heart Foundation RG/12/6/29670
6 · The paper itself

Abstract

Sympathetic activity displays rhythmic oscillations generated by brainstem inspiratory and expiratory neurons. Amplification of these rhythmic respiratory-related oscillations is observed in rats under enhanced central respiratory drive or during development of neurogenic hypertension. Herein, we evaluated the involvement of ventral medullary sympatho-excitatory catecholaminergic C1 neurons, using inhibitory Drosophila allatostatin receptors, for the enhanced expiratory-related oscillations in sympathetic activity in rats submitted to chronic intermittent hypoxia (CIH) and following activation of both peripheral (hypoxia) and central chemoreceptors (hypercapnia). Pharmacogenetic inhibition of C1 neurons bilaterally resulted in reductions of their firing frequency and amplitude of inspiratory-related sympathetic activity in rats in normocapnia, hypercapnia or after CIH. In contrast, hypercapnia or hypoxia-induced enhanced expiratory-related sympathetic oscillations were unaffected by C1 neuronal inhibition. Inhibition of C1 neurons also resulted in a significant fall in arterial pressure and heart rate that was similar in magnitude between normotensive and CIH hypertensive rats, but basal arterial pressure in CIH rats remained higher compared to controls. C1 neurons play a key role in regulating inspiratory modulation of sympathetic activity and arterial pressure in both normotensive and CIH hypertensive rats, but they are not involved in the enhanced late-expiratory-related sympathetic activity triggered by activation of peripheral or central chemoreceptors.

Indexed as

AnimalsBaroreflexBlood PressureDisease Models, AnimalDrosophilaDrosophila ProteinsGenetic VectorsHeart RateHomeodomain ProteinsHypercapniaHypertensionHypoxiaMaleMedulla OblongataNeuronsPatch-Clamp TechniquesAstA-R1 protein, DrosophilaDrosophila ProteinsHomeodomain ProteinsPhox2a protein, ratReceptors, G-Protein-CoupledReceptors, Neuropeptide

Identifiers

PMID29203815
PMCPMC5715015
OpenAlexW2769673202

What OpenQuestion holds

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LicenceCC BY
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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.