Efeitos cardiovasculares ao tratamento crônico com vitamina C na hipertensão renovascular em ratos Wistar

• Ano de defesa: 2010
• Autor(a) principal: Nishi, Erika Emy [UNIFESP]
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal de São Paulo (UNIFESP)
• Palavras-chave em Português: Controle reflexo barorreceptor; Atividade simpática renal; Vitamina C; Losartan; Hipertensão renovascular; Ácido ascórbico; Barorreflexo; Renal sympathetic nerve activity; Baroreceptor reflex; Vitamin C; Hypertension, renovascular; Ascorbic acid; Baroreflex
• Link de acesso: http://repositorio.unifesp.br/handle/11600/9387

Sympathetic vasomotor hyperactivity and baroreflex dysfunction are involved in the development and maintenance of Goldblatt 2 kidney, 1 clip (2K-1C) model of renovascular arterial hypertension (AH). This experimental model of AH is reninangiotensin system activation-dependent and the interaction of angiotensin (Ang) II with its subtype 1 receptor (AT1) activates the NAD(P)H oxidases enzymes, increasing superoxide anion production. We hypothesized that oxidative stress contributes to cardiovascular dysfunctions in the 2K-1C model. The aim of the present study was to evaluate the effects of chronic administration of an antioxidant, vitamin C (Vit C - 150 mg/kg/day) on mean arterial pressure (MAP), baroreceptor reflex (BR) and renal sympathetic nerve activity (rSNA) in male Wistar 2K-1C rats. Comparatively, the same cardiovascular parameters were evaluated under the effect of chronic treatment with AT1R blocker, losartan (Los - 30 mg/kg/day). Moreover, gene expressions (messenger RNA) of AT1, NAD(P)H oxidase subunits (p47phox and gp91phox) and the main antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were evaluated in the renal cortex as renal oxidative stress markers. Vit C treatment decreased basal MAP and rSNA only in the hypertensive group, increased cardiac BR gain to the bradycardic response (vagal component) and improved renal BR sensibility in control and 2K-1C groups, more intensely in hypertensive group. Addionally, Vit C decreased AT1 gene expression only in the clipped kidney and augmented GPx expression in both kidneys of hypertensive group. Los treatment normalized PAM and rSNA and increased cardiac BR to the bradycardic response only in the hypertensive group and improved renal BR more intensely in 2K-1C group. Therefore, the present study showed that chronic Vit C treatment improved hypertension and the control of baroreceptor reflex to the heart and the rSNA associated with reduced gene expression of AT1 and increased GPx expression in the ischemc kidney. Taken altogether, these data suggest a role for oxidative stress and rSNA in the maintenance of Ang II-dependent AH.