Han, S.Uludag, M.O.Usanmaz, S.E.Ayaloglu-Butun F.Akcali, K.C.Demirel-Yilmaz, E.2016-02-082016-02-0820150301-4851http://hdl.handle.net/11693/23270Hypertension is a risk factor for the cardiovascular diseases. Although, several drugs are used to treat hypertension, the success of the antihypertensive therapy is limited. Resveratrol decreases blood pressure in animal models of hypertension. This study researched the mechanisms behind the effects of resveratrol on hypertension. Hypertension was induced by using the deoxycorticosterone acetate (DOCA)-induced (15 mg/kg twice per week, subcutaneously) salt-sensitive hypertension model of Wistar rats. Hypertension caused a decrease in endothelium-dependent relaxations of the isolated thoracic aorta. Resveratrol treatment (50 mg/l in drinking water) prevented DOCA salt-induced hypertension, but did not improve endothelial dysfunction. Plasma nitric oxide (NO), asymmetric dimethylarginine (ADMA), total antioxidant capacity (TAC) and hydrogen sulfide (H2S) levels were not changed by DOCA salt application. However, treatment of resveratrol significantly decreased ADMA and increased TAC and H2S levels. NO level in circulation was not significantly changed by resveratrol. DOCA salt application and resveratrol treatment also caused an alteration in the epigenetic modification of vessels. Staining pattern of histone 3 lysine 27 methylation (H3K27me3) in the aorta and renal artery sections was changed. These results show that preventive effect of resveratrol on DOCA salt-induced hypertension might due to its action on the production of some blood biomarkers and the epigenetic modification of vessels that would focus upon new aspect of hypertension prevention and treatment. © 2014, Springer Science+Business Media Dordrecht.EnglishBiomarkerEndotheliumEpigenetic modificationHypertensionResveratrolhistone 3 lysine 27histone H3hydrogen sulfiden(g),n(g) dimethylargininenitric oxideresveratrolunclassified druganimal experimentanimal modelanimal tissueantioxidant activityArticlecontrolled studydeoxycorticosterone-salt induced hypertensionhistone methylationmalenonhumanratrenal arterythoracic aortavascular endotheliumvasodilatationArticle10.1007/s11033-014-3737-x