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dc.contributor.author Sára Levente
dc.contributor.author Nádasy György László
dc.contributor.author Antal P
dc.contributor.author Szekeres Mária
dc.contributor.author Monori-Kiss, Anna
dc.contributor.author Horvath Eszter Mária
dc.contributor.author Tőkés Anna-Mária
dc.contributor.author Masszi Gabriella
dc.contributor.author Monos Emil
dc.contributor.author Várbíró Szabolcs
dc.date.accessioned 2015-01-14T16:04:40Z
dc.date.available 2015-01-14T16:04:40Z
dc.date.issued 2012
dc.identifier 84866562058
dc.identifier.citation pagination=279-288; journalVolume=99; journalIssueNumber=3; journalTitle=ACTA PHYSIOLOGICA HUNGARICA;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/969
dc.identifier.uri doi:10.1556/APhysiol.99.2012.3.5
dc.description.abstract To clarify the effects of dihydrotestosterone (DHT)-induced polycystic ovary syndrome (PCOS) on arteriolar biomechanics in a rat model and the possible modulatory role of vitamin D3. METHODS AND RESULTS: The PCOS model was induced in female Wistar rats by ten-weeks DHT treatment. Arteriolar biomechanics was tested in arterioles by pressure arteriography in control as well as DHT- and DHT with vitamin D3-treated animals in contracted and passive conditions. Increased wall stress and distensibility as well as increased vascular lumen were detected after DHT treatment. Concomitant vitamin D3 treatment lowered the mechanical load of the arterioles and restored the vascular diameter. CONCLUSION: The hyperandrogenic state resulted in more rigid, less flexible arteriolar walls with increased vascular lumen compared with controls. DHT treatment caused eutrophic remodelling of gracilis arteriole. These prehypertensive alterations caused by chronic DHT treatment were mostly reversed by concomitant vitamin D3 administration.
dc.relation.ispartof urn:issn:0231-424X
dc.title Arteriolar biomechanics in a rat polycystic ovary syndrome model - Effects of parallel vitamin D3 treatment
dc.type Journal Article
dc.date.updated 2015-01-08T09:56:18Z
dc.language.rfc3066 en
dc.identifier.mtmt 2024577
dc.identifier.wos 000308759000005
dc.identifier.pubmed 22982716
dc.contributor.department SE/ÁOK/I/Élettani Intézet
dc.contributor.department SE/ÁOK/K/II. Sz. Szülészeti és Nőgyógyászati Klinika
dc.contributor.department SE/ÁOK/I/II. Sz. Patológiai Intézet
dc.contributor.department SE/ÁOK/I/Klinikai Kísérleti Kutató- és Humán Élettani Intézet
dc.contributor.institution Semmelweis Egyetem


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