Evidence map›Paper›PMID 23967142›Full record

ArticlePloS one2013

The effects of angiotensin II and angiotensin-(1-7) in the rostral ventrolateral medulla of rats on stress-induced hypertension.

Dongshu Du, Jun Chen, Min Liu, Minxia Zhu, Haojia Jing, Jie Fang, Linlin Shen, Danian Zhu, Jerry Yu, Jin Wang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

14 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Nav1.6 in the vasomotor center is a promising key molecule in the pathophysiology of stress-induced hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2019
    Article
  7. Review
  8. Review
  9. Upregulation of ATFrontiers in physiology · 2018
    Article
  10. Article
  11. Angiotensin-(1-7) in Paraventricular Nucleus Contributes to the Enhanced Cardiac Sympathetic Afferent Reflex and Sympathetic Activity in Chronic Heart Failure Rats.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2017
    Article
  12. Article
  13. Article
  14. Central involvement of SARS-CoV-2 may aggravate ARDS and hypertension.Journal of the renin-angiotensin-aldosterone system : JRAAS
    Article
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

10 authors at 2 institutions in 2 countries.

Dongshu DuDepartment of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai, China.
Jun Chen
Min Liu
Minxia Zhu
Haojia Jing
Jie Fang
Linlin Shen
Danian Zhu
Jerry Yu
Jin Wang
Shanghai Medical College of Fudan University · CNUniversity of Louisville · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have shown that angiotensin II (Ang II) and angiotensin-(1-7) [Ang-(1-7)] increased arterial blood pressure (BP) via glutamate release when microinjected into the rostral ventrolateral medulla (RVLM) in normotensive rats (control). In the present study, we tested the hypothesis that Ang II and Ang-(1-7) in the RVLM are differentially activated in stress-induced hypertension (SIH) by comparing the effects of microinjection of Ang II, Ang-(1-7), and their receptor antagonists on BP and amino acid release in SIH and control rats. We found that Ang II had greater pressor effect, and more excitatory (glutamate) and less inhibitory (taurine and γ-aminobutyric acid) amino acid release in SIH than in control animals. Losartan, a selective AT₁ receptor (AT₁R) antagonist, decreased mean BP in SIH but not in control rats. PD123319, a selective AT₂ receptor (AT₂R) antagonist, increased mean BP in control but not in SIH rats. However, Ang-(1-7) and its selective Mas receptor antagonist Ang779 evoked similar effects on BP and amino acid release in both SIH and control rats. Furthermore, we found that in the RVLM, AT₁R, ACE protein expression (western blot) and ACE mRNA (real-time PCR) were significantly higher, whereas AT₂R protein, ACE2 mRNA and protein expression were significantly lower in SIH than in control rats. Mas receptor expression was similar in the two groups. The results support our hypothesis and demonstrate that upregulation of Ang II by AT₁R, not Ang-(1-7), system in the RVLM causes hypertension in SIH rats by increasing excitatory and suppressing inhibitory amino acid release.

Indexed as

Amino AcidsAngiotensin IAngiotensin IIAnimalsAntihypertensive AgentsBlood PressureGene Expression RegulationHeart RateHypertensionMaleMedulla OblongataPeptide FragmentsPeptidyl-Dipeptidase ARatsRats, WistarReceptor, Angiotensin, Type 1Amino AcidsAngiotensin Iangiotensin I (1-7)Angiotensin IIAntihypertensive AgentsPeptide FragmentsPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 1

Identifiers

PMID23967142
PMCPMC3743893
OpenAlexW1980435282

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.