Evidence map›Paper›PMID 27432866›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Spironolactone Prevents Endothelial Nitric Oxide Synthase Uncoupling and Vascular Dysfunction Induced by β-Adrenergic Overstimulation: Role of Perivascular Adipose Tissue.

Jamaira A Victorio, Stefano P Clerici, Roberto Palacios, María J Alonso, Dalton V Vassallo, Iris Z Jaffe, Luciana V Rossoni, Ana P Davel

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

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Blood Pressure-Lowering Therapy.Handbook of experimental pharmacology · 2022
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Cellular mechanisms underlying obesity-induced arterial stiffness.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Cardioprotective Action ofFrontiers in pharmacology · 2017
    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

8 authors at 1 institution in 1 country.

Jamaira A VictorioFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
Stefano P ClericiFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
Roberto PalaciosFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
María J AlonsoFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
Dalton V VassalloFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
Iris Z JaffeFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
Luciana V RossoniFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.).
Ana P DavelFrom the Department of Structural and Functional Biology, Institute of Biology, University of Campinas, Brazil (J.A.V., S.P.C., A.P.D.); Department of Ciencias Básicas de la Salud, Universidad Rey Juan Carlos, Alcorcón, Spain (R.P., M.J.A.); Department of Physiological Sciences, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil (D.V.V.); Molecular Cardiology Research Institute, Tufts Medical Center, Boston, MA (I.Z.J.); and Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of São Paulo, Brazil (L.V.R.). anadavel@unicamp.br.
Tufts Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sustained stimulation of β-adrenoceptors (β-ARs) and activation of renin-angiotensin-aldosterone system are common features of cardiovascular diseases with rising sympathetic activation, including essential hypertension, myocardial infarction, and heart failure. In this study, we investigated the role of AT1 receptor and mineralocorticoid receptor (MR) in the vascular alterations caused by β-AR overstimulation. β-AR overstimulation with associated cardiac hypertrophy and increased vasoconstrictor response to phenylephrine in aorta were modeled in rats by 7-day isoproterenol treatment. The increased vasoconstrictor response to phenylephrine in this model was blunted by the MR antagonist spironolactone, but not by the AT1 receptor antagonist losartan, despite the blunting of cardiac hypertrophy with both drugs. Spironolactone, but not losartan, restored NO bioavailability in association with lower endothelial nitric oxide synthase-derived superoxide production, increased endothelial nitric oxide synthase dimerization, and aortic HSP90 upregulation. MR genomic and nongenomic functions were activated in aortas from isoproterenol-treated rats. Isoproterenol did not modify plasma levels of MR ligands aldosterone and corticosterone but rather increased perivascular adipose tissue-derived corticosterone in association with increased expression of 11β-hydroxysteroid dehydrogenase type 1. The anticontractile effect of aortic perivascular adipose tissue was impaired by β-AR overstimulation and restored by MR blockade. These results suggest that activation of vascular MR signaling contributes to the vascular dysfunction induced by β-AR overstimulation associated with endothelial nitric oxide synthase uncoupling. These findings reveal an additional explanation for the protective effects of MR antagonists in cardiovascular disorders with sympathetic activation.

Indexed as

Adipose TissueAnalysis of VarianceAnimalsCardiomegalyDisease Models, AnimalIsoproterenolLosartanMaleNitric Oxide Synthase Type IIIRandom AllocationRatsRats, WistarReceptors, MineralocorticoidRenin-Angiotensin SystemRoleSpironolactoneIsoproterenolLosartanNitric Oxide Synthase Type IIIReceptors, MineralocorticoidSpironolactoneadipose tissueaortalosartanmineralocorticoid receptor

Identifiers

PMID27432866
PMCPMC4978608
OpenAlexW2486430289

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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.