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Fructose intake exacerbates the contractile response elicited by norepinephrine in mesenteric vascular bed of rats via increased endothelial prostanoids.
Sousa, Glauciene J; Oliveira, Phablo Wendell C; Nogueira, Breno V; Melo, Antônio F; Faria, Thaís de Oliveira; Meira, Eduardo Frizera; Mill, José G; Bissoli, Nazaré S; Baldo, Marcelo P.
Afiliação
  • Sousa GJ; Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil.
  • Oliveira PWC; Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil.
  • Nogueira BV; Department of Morphology, Federal University of Espírito Santo, Vitória, Espírito Santo, Brazil.
  • Melo AF; Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil.
  • Faria TO; Department of Pathophysiology, Montes Claros State University, Montes Claros, Brazil.
  • Meira EF; Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil; Department of Pharmacy and Nutrition, Federal University of Espírito Santo, Alegre, Brazil.
  • Mill JG; Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil.
  • Bissoli NS; Department of Physiological Sciences, Federal University of Espírito Santo, Vitória, Brazil.
  • Baldo MP; Department of Pathophysiology, Montes Claros State University, Montes Claros, Brazil. Electronic address: marcelobaldo@ymail.com.
J Nutr Biochem ; 48: 21-28, 2017 10.
Article em En | MEDLINE | ID: mdl-28654829
Chronic fructose intake induces major cardiovascular and metabolic disturbances and is associated with the development of hypertension due to changes in vascular function. We hypothesized that high fructose intake for 6 weeks would cause metabolic syndrome and lead to initial vascular dysfunction. Male Wistar rats were assigned to receive fructose (FRU, 10%) or drinking water (CON) for 6 weeks. Systolic blood pressure was evaluated by tail plethysmography. Fasting glucose, insulin and glucose tolerance were measured at the end of the follow-up. Mesenteric vascular bed reactivity was tested before and after pharmacological blockade. Western blot analysis was performed for iNOS, eNOS, Nox2 and COX-2. DHE staining was used for vascular superoxide anion detection. Vessel structure was evaluated by optical and electronic microscopy. Fructose intake did not alter blood pressure, but did increase visceral fat deposition and fasting glucose as well as impair insulin and glucose tolerance. Fructose increased NE-induced vasoconstriction compared with CON, and this difference was abrogated by indomethacin perfusion as well as endothelium removal. ACh-induced relaxation was preserved, and the NO modulation tested after L-NAME perfusion was similar between groups. SNP-induced relaxation was not altered. Inducible NOS was increased; however, there were no changes in eNOS, Nox2 or COX-2 protein expression. Basal or stimulated superoxide anion production was not changed by fructose intake. In conclusion, high fructose intake increased NE-induced vasoconstriction through the endothelial prostanoids even in the presence of a preserved endothelium-mediated relaxation. No major changes in vessel structure were detected.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Endotélio Vascular / Norepinefrina / Prostaglandinas / Frutose Limite: Animals Idioma: En Revista: J Nutr Biochem Assunto da revista: BIOQUIMICA / CIENCIAS DA NUTRICAO Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Endotélio Vascular / Norepinefrina / Prostaglandinas / Frutose Limite: Animals Idioma: En Revista: J Nutr Biochem Assunto da revista: BIOQUIMICA / CIENCIAS DA NUTRICAO Ano de publicação: 2017 Tipo de documento: Article País de afiliação: Brasil País de publicação: Estados Unidos