Evidence map›Paper›PMID 27080540›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS

Increased vascular sympathetic modulation in mice with Mas receptor deficiency.

Karina Rabello Casali, Daniela Ravizzoni Dartora, Marina Moura, Mariane Bertagnolli, Michael Bader, Andrea Haibara, Natalia Alenina, Maria Claudia Irigoyen, Robson A Santos

Abstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS. 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
–field-weighted citation impact
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.

  1. Article
  2. Article
  3. Article
  4. The antiobese effect of AT1 receptor blockade is augmented in mice lacking Mas.Naunyn-Schmiedeberg's archives of pharmacology · 2019
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Angiotensin-(1-7) relieved renal injury induced by chronic intermittent hypoxia in rats by reducing inflammation, oxidative stress and fibrosis.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017
    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

9 authors.

Karina Rabello CasaliUniversidade Federal de São Paulo, São Paulo, Brazil Instituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil.
Daniela Ravizzoni DartoraInstituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil.
Marina MouraMax-Delbruck Center for Molecular Medicine, Berlin, Germany.
Mariane BertagnolliCHU Sainte Justine Research, Montreal, Canada.
Michael BaderMax-Delbruck Center for Molecular Medicine, Berlin, Germany.
Andrea HaibaraMax-Delbruck Center for Molecular Medicine, Berlin, Germany.
Natalia AleninaMax-Delbruck Center for Molecular Medicine, Berlin, Germany.
Maria Claudia IrigoyenInstituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil Instituto do Coração (InCor), São Paulo, Brazil.
Robson A SantosInstituto de Cardiologia-Fundação Universitária de Cardiologia, Porto Alegre, RS, Brazil National Institute of Science and Technology in Nanobiopharmaceutics, Belo Horizonte, Brazil robsonsant@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe angiotensin-converting enzyme 2 (ACE2)/angiotensin (Ang)-(1-7)/Mas axis could modulate the heart rate (HR) and blood pressure variabilities (BPV) which are important predictors of cardiovascular risk and provide information about the autonomic modulation of the cardiovascular system. Therefore we investigated the effect of Mas deficiency on autonomic modulation in wild type and Mas-knockout (KO) mice.

methodsBlood pressure was recorded at high sample rate (4000 Hz). Stationary sequences of 200-250 beats were randomly chosen. Frequency domain analysis of HR and BPV was performed with an autoregressive algorithm on the pulse interval sequences and on respective systolic sequences.

resultsThe KO group presented an increase of systolic arterial pressure (SAP; 127.26±11.20 vs 135.07±6.98 mmHg), BPV (3.54±1.54 vs 5.87±2.12 mmHg(2)), and low-frequency component of systolic BPV (0.12±0.11 vs 0.47±0.34 mmHg(2)).

conclusionsThe deletion of Mas receptor is associated with an increase of SAP and with an increased BPV, indicating alterations in autonomic control. Increase of sympathetic vascular modulation in absence of Mas evidences the important role of Ang-(1-7)/Mas on cardiovascular regulation. Moreover, the absence of significant changes in HR and HRV can indicate an adaptation of autonomic cardiac balance. Our results suggest that the Ang-(1-7)/Mas axis seems more important in autonomic modulation of arterial pressure than HR.

Indexed as

AnimalsBlood VesselsHemodynamicsMaleMice, KnockoutProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-CoupledSympathetic Nervous SystemSystoleProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupledangiotensin-(1–7)autonomic modulationblood pressure variabilityheart rate variabilityMas receptorRenin–angiotensin system

Identifiers

PMID27080540
PMCPMC5843925

What OpenQuestion holds

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LicenceCC BY-NC
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.