Evidence map›Paper›PMID 24533142›Full record

ArticlePloS one2014

Mechanisms of improved aortic stiffness by arotinolol in spontaneously hypertensive rats.

Wugang Zhou, Mona Hong, Ke Zhang, Dongrui Chen, Weiqing Han, Weili Shen, Dingliang Zhu, Pingjin Gao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2014. 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
0.6field-weighted citation impact, top 38% 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, 7 citations in OpenAlex.

  1. Sex differences in mechanisms of arterial stiffness.British journal of pharmacology · 2019
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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

8 authors at 1 institution in 1 country.

Wugang ZhouDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Mona HongDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Ke ZhangDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Dongrui ChenDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Weiqing HanDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Weili ShenDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Dingliang ZhuDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Pingjin GaoDepartment of Hypertension, RuiJin Hospital, Shanghai Key Lab of Hypertension, Shanghai Institute of Hypertension, Shanghai Jiaotong University, School of Medicine, Shanghai, China.
Shanghai Institute of Hypertension · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesThis study investigates the effects on aortic stiffness and vasodilation by arotinolol and the underlying mechanisms in spontaneously hypertensive rats (SHR).

methodsThe vasodilations of rat aortas, renal and mesenteric arteries were evaluated by isometric force recording. Nitric oxide (NO) was measured in human aortic endothelial cells (HAECs) by fluorescent probes. Sixteen-week old SHRs were treated with metoprolol (200 mg·kg-1·d⁻¹), arotinolol (30 mg·kg-1·d⁻¹) for 8 weeks. Central arterial pressure (CAP) and pulse wave velocity (PWV) were evaluated via catheter pressure transducers. Collagen was assessed by immunohistochemistry and biochemistry assay, while endothelial nitric oxide synthase (eNOS) and eNOS phosphorylation (p-eNOS) of HAECs or aortas were analyzed by western blotting.

resultsArotinolol relaxed vascular rings and the relaxations were attenuated by Nω-nitro-L-arginine methyl ester (L-NAME, NO synthase inhibitor) and the absence of endothelium. Furthermore, arotinolol-induced relaxations were attenuated by 4-aminopyridine (4-AP, Kv channels blocker). Arotinolol produced more nitric oxide compared to metoprolol and increased the expression of p-eNOS in HAECs. These results indicated that arotinolol-induced vasodilation involves endothelium-derived NO and Kv channels. The treatement with arotinolol in 8 weeks, but not metoprolol, markedly decreased CAP and PWV. Biochemistry assay and immunohistochemistry showed that aortic collagen depositions in the arotinolol groups were reduced compared with SHRs with metoprolol. Moreover, eNOS phosphorylation was significantly increased in aortinolol-treated SHR compared with SHRs with metoprolol.

conclusionsArotinolol improves arterial stiffness in SHR, which involved in increasing NO and decreasing collagen contents in large arteries.

Indexed as

AnimalsAortaCollagenHumansMaleMesenteric ArteriesMetoprololNitric OxideNitric Oxide Synthase Type IIIPhosphorylationPotassium ChannelsPropanolaminesRatsRats, Inbred SHRRenal ArteryVascular StiffnessarotinololCollagenMetoprololNitric OxideNitric Oxide Synthase Type IIIPotassium ChannelsPropanolamines

Identifiers

PMID24533142
PMCPMC3923047
OpenAlexW1987300040

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.