Brain Oxidative Stress in Neural Mechanism of Programmed Hypertension to Maternal High Fructose Diet

Abstract

Early life exposure to adverse environments can lead to a variety of adult diseases by a process referred to as developmental programming. Maternal high fructose diet (HFD) promotes programmed hypertension in adult offspring, although the underlying mechanism is not fully understood. Brain oxidative stress is pivotal in neural mechanism of hypertension. We tested in this study the hypothesis that brain oxidative stress contributes to programmed hypertension in adult offspring to maternal HFD. In normotensive rats, maternal HFD during gestation and lactation led to insulin resistance, increase in sympathetic activity and hypertension in the 3‐month‐old young offspring. This was associated with augmented neurogenic sympathetic vasomotor tone and high tissue levels of reactive oxygen species (ROS) at the brain stem. Maternal melatonin treatment or simvastatin treatment to the 2‐month‐old offspring significantly ameliorated oxidative stress in the brain stem of the offspring. Simvastatin treatment also abrogated sympathetic overexcitation and prevented the development of programmed hypertension in the 3‐month‐old rats to maternal HFD. These results suggest that brain stem oxidative stress may contribute to sympathoexcitation and programmed hypertension in the offspring to maternal HFD.This study was supported by grant (CMRPG8C0051) from Kaohsiung Chang Gung Memorial Hospital.