Evidence map›Paper›PMID 26907173›Full record

ArticlePloS one2016

Pharmacology of the Adenosine A3 Receptor in the Vasculature and Essential Hypertension.

Ming-Fen Ho, Leanne M Low, Roselyn B Rose'Meyer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.3field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Adenosine AInternational journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Purinergic Signalling: Therapeutic Developments.Frontiers in pharmacology · 2017
    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

3 authors at 1 institution in 1 country.

Ming-Fen HoHeart Foundation Research Centre, School of Medical Science, Griffith University, Gold Coast, Queensland, Australia.
Leanne M LowHeart Foundation Research Centre, School of Medical Science, Griffith University, Gold Coast, Queensland, Australia.
Roselyn B Rose'MeyerHeart Foundation Research Centre, School of Medical Science, Griffith University, Gold Coast, Queensland, Australia.
National Heart Foundation of Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEssential hypertension is considered to be a multifactorial disorder and its aetiology has yet to be clearly identified. As the adenosine receptors have a significant role in mediating vasodilation, alterations in their structures or signalling pathways may be involved in the development of hypertension. This study aimed to measure the expression of adenosine A3 receptors in a range of cardiovascular tissues and determine whether they could be altered with essential hypertension, and to functionally test responses to adenosine A3 receptor agonists in coronary blood vessels using the isolated perfused heart preparation.

methodsmRNA samples from cardiovascular tissues and a range of blood vessels were collected from 10 week old male spontaneously hypertensive rats and age-gender matched Wistar rats (n = 8). The Langendorff heart perfusion preparation was used to characterise adenosine A3 receptor mediated coronary vasodilation in the rat heart.

resultsAdenosine A3 receptor agonists induced coronary vasodilation. The expression of adenosine A3 receptors in cardiovascular tissues was altered in a tissue-specific pattern. Specifically, down-regulation of adenosine A3 receptor expression occurred in hypertensive hearts, which might be associated with attenuated vasodilator responses observed in coronary vessels to adenosine A3 receptor agonists.

conclusionsThis study demonstrated alterations in the expression of adenosine A3 receptors occurred in a tissue specific mode, and reduced adenosine A3 receptor mediated coronary vasodilation in hearts from spontaneously hypertensive rats. Our findings with regard to changes in the adenosine A3 receptor in hypertensive hearts suggest that adenosine A3 receptor might play a role in the physiopathology of essential hypertension and potentially open the way to pharmacologic manipulation of vasomotor activity by the use of adenosine A3 receptor agonists.

Indexed as

Adenosine A3 Receptor AgonistsAnimalsCoronary VesselsEssential HypertensionGene Expression RegulationHeartHypertensionMaleOrgan SpecificityRatsReceptor, Adenosine A3VasodilationAdenosine A3 Receptor AgonistsReceptor, Adenosine A3

Identifiers

PMID26907173
PMCPMC4764345
OpenAlexW2284990108

What OpenQuestion holds

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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.