Chronic high-sodium diet intake after weaning lead to neurogenic hypertension in adult Wistar rats

Abstract In this study, we investigated some mechanisms involved in sodium-dependent hypertension of rats exposed to chronic salt (NaCl) intake from weaning until adult age. Weaned male Wistar rats were placed under high (0.90% w/w, HS) or regular (0.27% w/w, Cont) sodium diets for 12 weeks. Water c...

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Autores principales: Paula Magalhães Gomes, Renato Willian Martins Sá, Giovana Lopes Aguiar, Milede Hanner Saraiva Paes, Andréia Carvalho Alzamora, Wanderson Geraldo Lima, Lisandra Brandino de Oliveira, Sean David Stocker, Vagner Roberto Antunes, Leonardo M. Cardoso
Formato: article
Lenguaje:EN
Publicado: Nature Portfolio 2017
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Acceso en línea:https://doaj.org/article/d658e42c252a449eb9413c1c226e50bd
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Sumario:Abstract In this study, we investigated some mechanisms involved in sodium-dependent hypertension of rats exposed to chronic salt (NaCl) intake from weaning until adult age. Weaned male Wistar rats were placed under high (0.90% w/w, HS) or regular (0.27% w/w, Cont) sodium diets for 12 weeks. Water consumption, urine output and sodium excretion were higher in HS rats compared to control. Blood pressure (BP) was directly measured by the arterial catheter and found 13.8% higher in HS vs Cont rats. Ganglionic blockade with hexamethonium caused greater fall in the BP of HS rats (33%), and central antagonism of AT1 receptors (losartan) microinjected into the lateral ventricle reduced BP level of HS, but not of Cont group. Heart rate variability analysis revealed sympathetic prevalence on modulation of the systolic interval. HS diet did not affect creatinine clearance. Kidney histological analysis revealed no significant change in renal corpuscle structure. Sodium and potassium concentrations in CSF were found higher in HS rats despite no change in plasma concentration of these ions. Taken together, data suggest that animals exposed to chronic salt intake to a level close to that reported for human’ diet since weaning lead to hypertension, which appears to rely on sodium-driven neurogenic mechanisms.