Reactive oxygen species derived from NAD(P)H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries
| العنوان: | Reactive oxygen species derived from NAD(P)H oxidase play a role on ethanol-induced hypertension and endothelial dysfunction in rat resistance arteries |
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| المؤلفون: | Natália A. Gonzaga, Camila A. Pereira, Rita C. Tostes, Ulisses V. Hipólito, Letícia N. Leite, Janaina A. Simplicio, Gabriel T. do Vale, Carlos R. Tirapelli |
| المصدر: | Repositório Institucional da USP (Biblioteca Digital da Produção Intelectual) Universidade de São Paulo (USP) instacron:USP |
| بيانات النشر: | Springer Science and Business Media LLC, 2016. |
| سنة النشر: | 2016 |
| مصطلحات موضوعية: | Male, medicine.medical_specialty, Nitric Oxide Synthase Type III, MAP Kinase Signaling System, Physiology, 030204 cardiovascular system & hematology, Biochemistry, Gene Expression Regulation, Enzymologic, Superoxide dismutase, Random Allocation, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Internal medicine, medicine, Animals, Enzyme Inhibitors, Phosphorylation, Rats, Wistar, Endothelial dysfunction, GLICOPROTEÍNAS DA MEMBRANA, chemistry.chemical_classification, Reactive oxygen species, Membrane Glycoproteins, biology, Chemistry, Superoxide, Acetophenones, NADPH Oxidases, NOX4, General Medicine, medicine.disease, Mesenteric Arteries, Alcoholism, Disease Models, Animal, Oxidative Stress, Endocrinology, Cardiovascular Diseases, Catalase, NAD(P)H oxidase, Hypertension, NADPH Oxidase 2, Apocynin, biology.protein, Cytokines, Vascular Resistance, Endothelium, Vascular, Reactive Oxygen Species, 030217 neurology & neurosurgery |
| الوصف: | Chronic ethanol consumption is a risk factor for cardiovascular diseases. We studied whether NAD(P)H oxidase-derived reactive oxygen species (ROS) play a role in ethanol-induced hypertension, vascular dysfunction, and protein expression in resistance arteries. Male Wistar rats were treated with ethanol (20 % v/v) for 6 weeks. Ethanol treatment increased blood pressure and decreased acetylcholine-induced relaxation in the rat mesenteric arterial bed (MAB). These responses were attenuated by apocynin (30 mg/kg/day; p.o. gavage). Ethanol consumption increased superoxide anion (O2−) generation and decreased nitrate/nitrite (NOx) concentration in the rat MAB and apocynin prevented these responses. Conversely, ethanol did not affect the concentration of hydrogen peroxide (H2O2) and reduced glutathione (GSH) or the activity of superoxide dismutase (SOD) and catalase (CAT) in the rat MAB. Ethanol increased interleukin (IL)-10 levels in the rat MAB but did not affect the levels of tumor necrosis factor (TNF)-α, IL-6, or IL-1β. Ethanol increased the expression of Nox2 and the phosphorylation of SAPK/JNK, but reduced eNOS expression in the rat MAB. Apocynin prevented these responses. However, ethanol treatment did not affect the expression of Nox1, Nox4, p38MAPK, ERK1/2, or SAPK/JNK in the rat MAB. Ethanol increased plasma levels of TBARS, TNF-α, IL-6, IL-1β, and IL-10, whereas it decreased NOx levels. The major finding of our study is that NAD(P)H oxidase-derived ROS play a role on ethanol-induced hypertension and endothelial dysfunction in resistance arteries. Moreover, ethanol consumption affects the expression and phosphorylation of proteins that regulate vascular function and NAD(P)H oxidase-derived ROS play a role in such responses. |
| تدمد: | 1877-8755 1138-7548 |
| DOI: | 10.1007/s13105-016-0519-z |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c93935d6f1ec5592cd61340171eb8c29 https://doi.org/10.1007/s13105-016-0519-z |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....c93935d6f1ec5592cd61340171eb8c29 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 18778755 11387548 |
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| DOI: | 10.1007/s13105-016-0519-z |