Evidence map›Paper›PMID 22563439›Full record

ArticlePloS one2012

Mechanisms of endothelial dysfunction in resistance arteries from patients with end-stage renal disease.

Leanid Luksha, Peter Stenvinkel, Folke Hammarqvist, Juan Jesús Carrero, Sandra T Davidge, Karolina Kublickiene

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Trial
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  9. Pre-clinical model of severe glutathione peroxidase-3 deficiency and chronic kidney disease results in coronary artery thrombosis and depressed left ventricular function.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2018
    Article
  10. Article
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  13. αKlotho and vascular calcification: an evolving paradigm.Current opinion in nephrology and hypertension · 2014
    Review
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  15. Article
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  17. Endothelial cell transfusion ameliorates endothelial dysfunction in 5/6 nephrectomized rats.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  18. 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

6 authors at 3 institutions in 2 countries.

Leanid LukshaDivision of Obstetrics & Gynecology, Karolinska Institutet, Karolinska University Hospital, Department of Clinical Science, Intervention & Technology, Stockholm, Sweden.
Peter Stenvinkel
Folke Hammarqvist
Juan Jesús Carrero
Sandra T Davidge
Karolina Kublickiene
Karolinska University Hospital · SEKarolinska Institutet · SEUniversity of Alberta · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

The study focuses on the mechanisms of endothelial dysfunction in the uremic milieu. Subcutaneous resistance arteries from 35 end-stage renal disease (ESRD) patients and 28 matched controls were studied ex-vivo. Basal and receptor-dependent effects of endothelium-derived factors, expression of endothelial NO synthase (eNOS), prerequisites for myoendothelial gap junctions (MEGJ), and associations between endothelium-dependent responses and plasma levels of endothelial dysfunction markers were assessed. The contribution of endothelium-derived hyperpolarizing factor (EDHF) to endothelium-dependent relaxation was impaired in uremic arteries after stimulation with bradykinin, but not acetylcholine, reflecting the agonist-specific differences. Diminished vasodilator influences of the endothelium on basal tone and enhanced plasma levels of asymmetrical dimethyl L-arginine (ADMA) suggest impairment in NO-mediated regulation of uremic arteries. eNOS expression and contribution of MEGJs to EDHF type responses were unaltered. Plasma levels of ADMA were negatively associated with endothelium-dependent responses in uremic arteries. Preserved responses of smooth muscle to pinacidil and NO-donor indicate alterations within the endothelium and tolerance of vasodilator mechanisms to the uremic retention products at the level of smooth muscle. We conclude that both EDHF and NO pathways that control resistance artery tone are impaired in the uremic milieu. For the first time, we validate the alterations in EDHF type responses linked to kinin receptors in ESRD patients. The association between plasma ADMA concentrations and endothelial function in uremic resistance vasculature may have diagnostic and future therapeutic implications.

Indexed as

AdultAgedArginineArteriesBiological FactorsBradykininEndothelium, VascularFemaleGap JunctionsHumansKidney Failure, ChronicMaleMiddle AgedNitric Oxide Synthase Type IIIVasodilator AgentsArginineBiological FactorsBradykinindimethylarginineendothelium-dependent hyperpolarization factorNitric Oxide Synthase Type IIIVasodilator Agents

Identifiers

PMID22563439
PMCPMC3338576
OpenAlexW2005588918

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.