Egyszerű nézet

dc.contributor OTKA:K-101775
dc.contributor SE ÁOK Dékán: Pál, Éva Hadjad, Leila Fontányi, Zoltán Monori-Kiss, Anna Mezei, Zsuzsanna Magyar, Attila Heinzlmann, Andrea Karvaly, Gellért Balázs Monos, Emil Nádasy, György László Benyó, Zoltán Várbíró, Szabolcs 2018-04-12T09:20:27Z 2018-04-12T09:20:27Z 2018
dc.identifier.citation pagination=e0192480, pages: 16; journalVolume=13; journalIssueNumber=2; journalTitle=PLOS ONE;
dc.identifier.uri doi:10.1371/journal.pone.0192480
dc.description.abstract BACKGROUND AND PURPOSE: Vitamin 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. METHODS: Four-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. RESULTS: VDD 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. CONCLUSIONS: VDD 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.
dc.relation.ispartof urn:issn:1932-6203
dc.title Vitamin D deficiency causes inward hypertrophic remodeling and alters vascular reactivity of rat cerebral arterioles
dc.type Journal Article 2018-02-22T09:31:02Z
dc.language.rfc3066 en
dc.identifier.mtmt 3333552
dc.identifier.pubmed 29408903
dc.contributor.department SE/KSZE/Klinikai Kísérleti Kutató Intézet
dc.contributor.department SE/AOK/I/Anatómiai, Szövet- és Fejlődéstani Intézet
dc.contributor.department SE/AOK/I/Élettani Intézet
dc.contributor.department SE/AOK/K/II. Sz. Szülészeti és Nőgyógyászati Klinika
dc.contributor.institution Semmelweis Egyetem

Kapcsolódó fájlok:

A fájl jelenleg csak egyetemi IP címről érhető el.


Ez a rekord az alábbi gyűjteményekben szerepel:

Egyszerű nézet