Evidence map›Paper›PMID 28877652›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS

Angiotensin-(1-7) attenuates atrial tachycardia-induced sympathetic nerve remodeling.

Wenfeng Shangguan, Wen Shi, Guangping Li, Yuanyuan Wang, Jian Li, Xuewen Wang

Open access · hybridAbstract 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.2field-weighted citation impact, top 39% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. The renin-angiotensin system in cardiovascular autonomic control: recent developments and clinical implications.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2019
    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

6 authors at 2 institutions in 1 country.

Wenfeng ShangguanTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, China.
Wen ShiTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, China.
Guangping LiTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, China.
Yuanyuan WangTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, China.
Jian LiTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, China.
Xuewen WangTianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, China.
Second Hospital of Tianjin Medical University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe effect of Angiotensin-(1-7) (Ang-(1-7)) on atrial autonomic remodeling is still unknown. We hypothesized that Ang-(1-7) could inhibit sympathetic nerve remodeling in a canine model of chronic atrial tachycardia. MATERIALS AND

methodsEighteen dogs were randomly assigned to sham group, pacing group and Ang-(1-7) group. Rapid atrial pacing was maintained for 14 days in the pacing and Ang-(1-7) groups. Ang-(1-7) was administered intravenously in the Ang-(1-7) group. The atrial effective refractory period and atrial fibrillation inducibility level were measured at baseline and under sympathetic nerve stimulation after 14 days of measurement. The atrial sympathetic nerves labeled with tyrosine hydroxylase were detected using immunohistochemistry and Western blotting, and tyrosine hydroxylase and nerve growth factor mRNA levels were measured by reverse transcription polymerase chain reaction.

resultsPacing shortened the atrial effective refractory period and increased the atrial fibrillation inducibility level at baseline and under sympathetic nerve stimulation. Ang-(1-7) treatment attenuated the shortening of the atrial effective refractory period and the increase in the atrial fibrillation inducibility level. Immunohistochemistry and Western blotting showed sympathetic nerve hyperinnervation in the pacing group, while Ang-(1-7) attenuated sympathetic nerve proliferation. Ang-(1-7) alleviated the pacing-induced increases in tyrosine hydroxylase and nerve growth factor mRNA expression levels.

conclusionAng-(1-7) can attenuate pacing-induced atrial sympathetic hyperinnervation.

Indexed as

Angiotensin IAnimalsAtrial FibrillationBlood PressureDogsFemaleHeart RateMaleNerve Growth FactorPeptide FragmentsRefractory Period, ElectrophysiologicalRNA, MessengerSympathetic Nervous SystemTachycardiaTyrosine 3-MonooxygenaseAngiotensin Iangiotensin I (1-7)Nerve Growth FactorPeptide FragmentsRNA, MessengerTyrosine 3-MonooxygenaseAngiotensin-(1–7)atrial fibrillationchronic atrial pacingsympathetic nerve remodelingtyrosine hydroxylase

Identifiers

PMID28877652
PMCPMC5843893
OpenAlexW2789136910

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.