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Abstract Aim: We investigated the effects of continuous or interval aerobic exercise training on vascular reactivity of female rats fed with fructose. Methods: Female Wistar rats (8-wk old) were divided into: sedentary (SD), continuous training (CTR), and interval training (ITR). Moderate intensity training protocols consisted of running 3 days/week for 7 weeks. CTR ran 40 min at 30%-40% of the maximal speed (MS) and TRI consisted of 7 sets of 1 min at 70% of MS followed by 3 min at 35% of MS. Animals were fed with standard chow and fructose (10%) in drinking water. Concentration-response curves to acetylcholine and phenylephrine, and oxidative stress biomarkers, were determined in the aorta. Body weight gain, visceral fat, and plasma triglycerides and glucose were also evaluated. Results: Endothelium-dependent relaxation was significantly increased by both exercise regimens (CTR: Emax = 85 ± 6% and ITR: Emax = 84 ± 1%) compared to sedentary rats (SD: Emax = 62 ± 5%). The contractile maximal response was not different but phenylephrine potency was increased in CTR (pEC50: 8.41 ± 0.19) and reduced in ITR (pEC50: 7.06 ± 0.11) compared to SD (pEC50: 7.77 ± 0.08). In addition, the generation of superoxide was lower in trained groups as compared with sedentary (about −28% in CTR and −22% in ITR). TBARS and nitrate/nitrite levels were not modified. Compared to the SD group, ITR gained 39% less body weight and CTR has 29% less visceral fat. Glucose and triglycerides were not modified. Conclusion: CTR and ITR, carried out 3 days/week, were efficient to improve endothelium-dependent relaxation and reduce superoxide generation in the aorta from female rats fed with fructose.
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Abstract Background: The mechanism underlying the vascular dysfunction induced by ethanol is not totally understood. Identification of biochemical/molecular mechanisms that could explain such effects is warranted. Objective: To investigate whether acute ethanol intake activates the vascular RhoA/Rho kinase pathway in resistance arteries and the role of NAD(P)H oxidase-derived reactive oxygen species (ROS) on such response. We also evaluated the requirement of p47phox translocation for ethanol-induced NAD(P)H oxidase activation. Methods: Male Wistar rats were orally treated with ethanol (1g/kg, p.o. gavage) or water (control). Some rats were treated with vitamin C (250 mg/kg, p.o. gavage, 5 days) before administration of water or ethanol. The mesenteric arterial bed (MAB) was collected 30 min after ethanol administration. Results: Vitamin C prevented ethanol-induced increase in superoxide anion (O2-) generation and lipoperoxidation in the MAB. Catalase and superoxide dismutase activities and the reduced glutathione, nitrate and hydrogen peroxide (H2O2) levels were not affected by ethanol. Vitamin C and 4-methylpyrazole prevented the increase on O2- generation induced by ethanol in cultured MAB vascular smooth muscle cells. Ethanol had no effect on phosphorylation levels of protein kinase B (Akt) and eNOS (Ser1177 or Thr495 residues) or MAB vascular reactivity. Vitamin C prevented ethanol-induced increase in the membrane: cytosol fraction ratio of p47phox and RhoA expression in the rat MAB. Conclusion: Acute ethanol intake induces activation of the RhoA/Rho kinase pathway by a mechanism that involves ROS generation. In resistance arteries, ethanol activates NAD(P)H oxidase by inducing p47phox translocation by a redox-sensitive mechanism.
Resumo Fundamento: O mecanismo da disfunção vascular induzido pelo consumo de etanol não é totalmente compreendido. Justifica-se, assim a identificação de mecanismos bioquímicos e moleculares que poderiam explicar tais efeitos. Objetivos: Investigar se a ingestão aguda de etanol ativa a via vascular RhoA/Rho quinase em artérias de resistência e o papel das espécies reativas de oxigênio (ERO) derivadas da NAD(P)H oxidase nessa resposta. Nós também avaliamos se ocorreu translocação da p47phox e ativação da NAD(P)H oxidase após o consumo agudo de etanol. Métodos: Ratos Wistar machos foram tratados com etanol via oral (1g/kg, p.o. gavagem) ou água (controle). Alguns ratos foram tratados com vitamina C (250 mg/kg, p.o. gavagem, 5 dias) antes de água ou etanol. O leito arterial mesentérico (LAM) foi coleado 30 min após a administração de etanol. Resultados: A vitamina C preveniu o aumento da geração de ânion superóxido (O2 -) e lipoperoxidação no LAM induzidos pelo etanol. A atividade da catalase (CAT), da superóxido dismutase (SOD) e os níveis de glutationa reduzida(GSH), nitrato e peróxido de hidrogênio (H2O2) não foram afetados após a ingestão aguda de etanol. A vitamina C e o 4-metilpirazol preveniram o aumento na geração de O2 - induzido pelo etanol em cultura de células do músculo liso vascular (CMLV). O etanol não afetou a fosforilação da proteína quinase B (Akt) e nem da óxido nítrico sintase endotelial (eNOS) (nos resíduos de Ser1177 ou Thr495) ou a reatividade vascular do LAM. A vitamina C preveniu o aumento da razão membrana:citosol da p47phox e a expressão da RhoA no LAM de rato induzido pelo etanol. Conclusão: A ingestão aguda de etanol induz a ativação da via RhoA/Rho quinase por um mecanismo que envolve a geração de ERO. Nas artérias de resistência, o etanol ativa NAD(P)H oxidase induzindo a translocação da p47phox por um mecanismo redox-sensível.