Autor: |
Carla S. Ceron, Gabriel T. do Vale, Janaina A. Simplicio, Patrícia Passaglia, Sthefany T. Ricci, Carlos R. Tirapelli |
Jazyk: |
angličtina |
Rok vydání: |
2017 |
Předmět: |
|
Zdroj: |
Data in Brief, Vol 11, Iss C, Pp 111-116 (2017) |
Druh dokumentu: |
article |
ISSN: |
2352-3409 |
DOI: |
10.1016/j.dib.2017.01.006 |
Popis: |
We describe the effects of losartan, a selective AT1 receptor antagonist on the alterations induced by treatment with ethanol in the rat aorta. The data shown here are related to the article entitled “Angiotensin type 1 receptor mediates chronic ethanol consumption-induced hypertension and vascular oxidative stress” (P. Passaglia, C.S. Ceron, A.S. Mecawi, J. Antunes-Rodrigues, E.B. Coelho, C.R. Tirapelli, 2015) [1]. Here we include new data on the protective effect of losartan against ethanol-induced oxidative stress. Male Wistar rats treated for 2 weeks with ethanol (20%, vol./vol.) exhibited increased aortic production of reactive oxygen species (ROS) and losartan (10 mg/kg/day; p.o. gavage) prevented this response. Ethanol did not alter the expression of eNOS in the rat aorta. Losartan prevented ethanol-induced increase in the aortic expression of nNOS. Neither ethanol nor losartan affected superoxide dismutase (SOD) or catalase (CAT) activities in the rat aorta. Treatment with ethanol increased the contraction induced by phenylephrine in both endothelium-intact and endothelium-denuded aortas and these responses were prevented by losartan. Conversely, neither ethanol nor losartan affected the endothelium-dependent relaxation induced by acetylcholine. |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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