Evidence map›Paper›PMID 29408903›Full record

ArticlePloS one2018

Vitamin D deficiency causes inward hypertrophic remodeling and alters vascular reactivity of rat cerebral arterioles.

Éva Pál, Leila Hadjadj, Zoltán Fontányi, Anna Monori-Kiss, Zsuzsanna Mezei, Norbert Lippai, Attila Magyar, Andrea Heinzlmann, Gellért Karvaly, Emil Monos and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. 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
2.2field-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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Improved hemodynamic and cardiorespiratory instability with vitamin D supplementation in an obstructive sleep apnea rat models.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
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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

13 authors at 1 institution in 1 country.

Éva PálInstitute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary.ORCID 0000-0003-1793-1912
Leila HadjadjInstitute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary.
Zoltán Fontányi2nd Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary.
Anna Monori-KissInstitute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary.
Zsuzsanna MezeiDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Norbert LippaiDepartment of Pathology, Jász-Nagykun-Szolnok County Hetényi Géza Hospital, Szolnok, Hungary.
Attila MagyarDepartment of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Andrea HeinzlmannDepartment of Anatomy, Histology and Embryology, Semmelweis University, Budapest, Hungary.
Gellért KarvalyDepartment of Laboratory Medicine, Semmelweis University, Budapest, Hungary.
Emil MonosInstitute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary.
György NádasyDepartment of Physiology, Semmelweis University, Budapest, Hungary.
Zoltán BenyóInstitute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary.
Szabolcs Várbíró2nd Department of Obstetrics and Gynecology, Semmelweis University, Budapest, Hungary.
Semmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeVitamin D deficiency (VDD) is a global health problem, which can lead to several pathophysiological consequences including cardiovascular diseases. Its impact on the cerebrovascular system is not well understood. The goal of the present work was to examine the effects of VDD on the morphological, biomechanical and functional properties of cerebral arterioles.

methodsFour-week-old male Wistar rats (n = 11 per group) were either fed with vitamin D deficient diet or received conventional rat chow with per os vitamin D supplementation. Cardiovascular parameters and hormone levels (testosterone, androstenedione, progesterone and 25-hydroxyvitamin D) were measured during the study. After 8 weeks of treatment anterior cerebral artery segments were prepared and their morphological, biomechanical and functional properties were examined using pressure microangiometry. Resorcin-fuchsin and smooth muscle actin staining were used to detect elastic fiber density and smooth muscle cell counts in the vessel wall, respectively. Sections were immunostained for eNOS and COX-2 as well.

resultsVDD markedly increased the wall thickness, the wall-to-lumen ratio and the wall cross-sectional area of arterioles as well as the number of smooth muscle cells in the tunica media. As a consequence, tangential wall stress was significantly lower in the VDD group. In addition, VDD increased the myogenic as well as the uridine 5'-triphosphate-induced tone and impaired bradykinin-induced relaxation. Decreased eNOS and increased COX-2 expression were also observed in the endothelium of VDD animals.

conclusionsVDD causes inward hypertrophic remodeling due to vascular smooth muscle cell proliferation and enhances the vessel tone probably because of increased vasoconstrictor prostanoid levels in young adult rats. In addition, the decreased eNOS expression results in endothelial dysfunction. These morphological and functional alterations can potentially compromise the cerebral circulation and lead to cerebrovascular disorders in VDD.

Indexed as

Vascular RemodelingAnimalsArteriolesBlood GlucoseCerebral ArteriesMaleRatsRats, WistarVitamin DVitamin D Deficiency25-hydroxyvitamin DBlood GlucoseVitamin D

Identifiers

PMID29408903
PMCPMC5800593
OpenAlexW2793442024

What Socratic holds

Textmetadata
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 Socratic graph.