Egyszerű nézet

dc.contributor.author Sugár, Dániel
dc.contributor.author Agócs, Róbert István
dc.contributor.author Tatár E
dc.contributor.author Tóth, Gergő
dc.contributor.author Horváth, Péter
dc.contributor.author Sulyok, Endre
dc.contributor.author Szabó, Attila
dc.date.accessioned 2021-04-29T10:48:38Z
dc.date.available 2021-04-29T10:48:38Z
dc.date.issued 2018
dc.identifier.citation journalVolume=67;journalIssueNumber=5;journalTitle=PHYSIOLOGICAL RESEARCH;pagerange=777-785;journalAbbreviatedTitle=PHYSIOL RES;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/6565
dc.description.abstract The glycosaminoglycan (GAG) molecules are a group of high molecular weight, negatively charged polysaccharides present abundantly in the mammalian organism. By their virtue of ion and water binding capacity, they may affect the redistribution of body fluids and ultimately the blood pressure. Data from the literature suggests that the mitogens Vascular Endothelial Growth Factor (VEGF)-A and VEGF-C are able to regulate the amount and charge density of GAGs and their detachment from the cell surface. Based on these findings we investigated the relationship between the level of dietary sodium intake, the expression levels of VEGF-A and VEGF-C, and the amount of the skin GAGs hyaluronic acid and chondroitin sulphate in an in vivo rat model. Significant correlation between dietary sodium intake, skin sodium levels and GAG content was found. We confirmed the GAG synthesizing role of VEGF-C but failed to prove that GAGs are degraded by VEGF-A. No significant difference in blood pressure was registered between the different dietary groups. A quotient calculated form the ion and water content of the skin tissue samples suggests that - in contrast to previous findings - the osmotically inactive ions and bound water fractions are proportional.
dc.format.extent 777-785
dc.relation.ispartof urn:issn:0862-8408
dc.title The contribution of skin glycosaminoglycans to the regulation of sodium homeostasis in rats
dc.type Journal Article
dc.date.updated 2018-11-20T10:52:59Z
dc.rights.holder NULL
dc.identifier.mtmt 3254337
dc.identifier.pubmed 28787171
dc.contributor.department SE/AOK/K/I. Sz. Gyermekgyógyászati Klinika
dc.contributor.department SE/GYTK/Gyógyszerészi Kémiai Intézet
dc.contributor.department SE/AOK/K/ISZGYK/MTA-SE Gyermekgyógyászati és Nephrológiai Kutatócsoport
dc.contributor.institution Semmelweis Egyetem


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