Evidence map›Paper›PMID 40377659›Full record

ArticlePflugers Archiv : European journal of physiology2025

Ethanol-induced dysfunction of the mesenteric perivascular adipose tissue is driven by mineralocorticoid receptors.

Ivis V O Martins, Thales M H Dourado, Gustavo F Pimenta, Marcela M Blascke de Mello, Aline G Fedoce, Wanessa M C Awata, Michele M Castro, Rita C Tostes, Carlos R Tirapelli

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

9 authors.

Ivis V O MartinsDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Thales M H DouradoDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Gustavo F PimentaDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Marcela M Blascke de MelloDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Aline G FedoceDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Wanessa M C AwataDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Michele M CastroDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Rita C TostesDepartamento de Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto, São Paulo, Brazil.
Carlos R TirapelliDepartamento de Ciências BioMoleculares, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, USP, Ribeirão Preto, São Paulo, Brazil. crtirapelli@usp.br.

Funding

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior Finance Code 001
6 · The paper itself

Abstract

The renin-angiotensin-aldosterone system (RAAS) is critical in ethanol-induced vascular dysfunction. Mineralocorticoid receptors (MR) trigger ethanol-induced vascular hypercontractility through pro-oxidative and pro-inflammatory effects. However, the contribution of MR to ethanol-induced perivascular adipose tissue (PVAT) dysfunction is unknown. Appreciating the importance of MR to PVAT dysfunction in distinctive pathological conditions, we investigated whether MR would play a role in ethanol-induced PVAT dysfunction. With this purpose, male Wistar Hannover rats were treated with ethanol 20% (in volume ratio) and/or potassium canrenoate [a MR antagonist (MRA); 30 mg/kg/day, gavage] for 5 weeks. Ethanol increased the circulating levels of aldosterone and impaired acetylcholine-induced relaxation of mesenteric arteries with, but not without PVAT. Antagonism of MR prevented ethanol-induced impairment in acetylcholine relaxation as well as the reduction of leptin levels and reactive oxygen species (ROS) overproduction in the mesenteric PVAT (mPVAT) from ethanol-treated rats. Ethanol promoted neutrophil accumulation and augmented the concentration of tumor necrosis factor (TNF)-α in the mPVAT and these responses were prevented by the MRA. Functional assays showed that tiron [a scavenger of superoxide (O

Indexed as

Adipose TissueEthanolMesenteric ArteriesReceptors, MineralocorticoidAldosteroneAnimalsMaleMesenteryMineralocorticoid Receptor AntagonistsRatsRats, WistarReactive Oxygen SpeciesTumor Necrosis Factor-alphaVasodilationAldosteroneEthanolMineralocorticoid Receptor AntagonistsReactive Oxygen SpeciesReceptors, MineralocorticoidTumor Necrosis Factor-alphaEthanolMineralocorticoid receptorsPerivascular adipose tissueTNF-αVascular dysfunction

Identifiers

PMID40377659

What Socratic holds

Textmetadata
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 Socratic graph.