Evidence map›Paper›PMID 28893245›Full record

ArticleJournal of biomedical science2017

Age-dependent redox status in the brain stem of NO-deficient hypertensive rats.

Miroslava Majzúnová, Zuzana Pakanová, Peter Kvasnička, Peter Bališ, Soňa Čačányiová, Ima Dovinová

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  6. Review
  7. Chronic L-Name-Treatment Produces Hypertension by Different Mechanisms in Peripheral Tissues and Brain: Role of Central eNOS.Pathophysiology : the official journal of the International Society for Pathophysiology · 2020
    Article
  8. Review
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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

6 authors at 3 institutions in 2 countries.

Miroslava MajzúnováInstitute of Normal and Pathological Physiology, Slovak Academy of Sciences, Sienkiewiczova 1, 813 71, Bratislava, Slovakia.
Zuzana PakanováInstitute of Chemistry, Slovak Academy of Sciences, Bratislava, Slovakia.
Peter KvasničkaInstitute of Particle and Nuclear Physics, Faculty of Mathematics and Physics, Charles University, Prague, Czech Republic.
Peter BališInstitute of Normal and Pathological Physiology, Slovak Academy of Sciences, Sienkiewiczova 1, 813 71, Bratislava, Slovakia.
Soňa ČačányiováInstitute of Normal and Pathological Physiology, Slovak Academy of Sciences, Sienkiewiczova 1, 813 71, Bratislava, Slovakia.
Ima DovinováInstitute of Normal and Pathological Physiology, Slovak Academy of Sciences, Sienkiewiczova 1, 813 71, Bratislava, Slovakia. Ima.Dovinova@savba.sk.ORCID http://orcid.org/0000-0001-9840-1950
Slovak Academy of Sciences · SKCharles University · CZInstitute of Chemistry of the Slovak Academy of Sciences · SK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe brain stem contains important nuclei that control cardiovascular function via the sympathetic nervous system (SNS), which is strongly influenced by nitric oxide. Its biological activity is also largely determined by oxygen free radicals. Despite many experimental studies, the role of AT1R-NAD(P)H oxidase-superoxide pathway in NO-deficiency is not yet sufficiently clarified. We determined changes in free radical signaling and antioxidant and detoxification response in the brain stem of young and adult Wistar rats during chronic administration of exogenous NO inhibitors.

methodsYoung (4 weeks) and adult (10 weeks) Wistar rats were treated with 7-nitroindazole (7-NI group, 10 mg/kg/day), a specific nNOS inhibitor, with N

resultsWe observed a blood pressure elevation and decrease in NOS activity only after L-NAME application in both age groups. Gene expression of nNOS (youngs) and eNOS (adults) in the brain stem decreased after both inhibitors. The radical signaling pathway triggered by AT1R and p22phox was elevated in L-NAME adults, but not in young rats. Moreover, L-NAME-induced NOS inhibition increased antioxidant response, as indicated by the observed elevation of mRNA SOD3, HO-1, AT2R and MDR1a in adult rats. 7-NI did not have a significant effect on AT1R-NADPH oxidase-superoxide pathway, yet it affected antioxidant response of mRNA expression of SOD1 and stimulated total activity of SOD in young rats and mRNA expression of AT2R in adult rats.

conclusionOur results show that chronic NOS inhibition by two different NOS inhibitors has age-dependent effect on radical signaling and antioxidant/detoxificant response in Wistar rats. While 7-NI had neuroprotective effect in the brain stem of young Wistar rats, L-NAME- induced NOS inhibition evoked activation of AT1R-NAD(P)H oxidase pathway in adult Wistar rats. Triggering of the radical pathway was followed by activation of protective compensation mechanism at the gene expression level.

Indexed as

Inactivation, MetabolicAge FactorsAnimalsAntioxidantsBrain StemEnzyme InhibitorsFree RadicalsIndazolesMaleNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseRatsRats, Wistar7-nitroindazoleAntioxidantsEnzyme InhibitorsFree RadicalsIndazolesNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthaseAntioxidant responseBrain stemNOS inhibitionRadical signaling

Identifiers

PMID28893245
PMCPMC5594586
OpenAlexW2754107262

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Registered trials

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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.