New Insights on the Maternal Diet Induced-Hypertension: Potential Role of the Phenotypic Plasticity and Sympathetic-Respiratory Overactivity.

Systemic arterial hypertension (SAH) is an important risk factor for cardiovascular disease and affects worldwide population. Current environment including life style coupled with genetic programming have been attributed to the rising incidence of hypertension. Besides, environmental conditions during perinatal development such as maternal malnutrition can program changes in the integration among renal, neural, and endocrine system leading to hypertension. This phenomenon is termed phenotypic plasticity and refers to the adjustment of a phenotype in response to environmental stimuli without genetic change, following a novel or unusual input during development. Human and animal studies indicate that fetal exposure to an adverse maternal environment may alter the renal morphology and physiology that contribute to the development of hypertension. Recently, it has been shown that the maternal protein restriction alter the central control of SAH by a mechanism that include respiratory dysfunction and enhanced sympathetic-respiratory coupling at early life, which may contribute to adult hypertension. This review will address the new insights on the maternal diet induced-hypertension that include the potential role of the phenotypic plasticity, specifically the perinatal protein malnutrition, and sympathetic-respiratory overactivity.

Short- and long-term effects of a maternal low-protein diet on ventilation, O2/CO2 chemoreception and arterial blood pressure in male rat offspring.

Maternal undernutrition increases the risk of adult arterial hypertension. The present study investigated the short- and long-term effects of a maternal low-protein diet on respiratory rhythm, O2/CO2 chemosensitivity and arterial blood pressure (ABP) of the offspring. Male Wistar rats were divided into two groups according to their mothers' diets during gestation and lactation: control (NP, 17% of casein) and low-protein (LP, 8% of casein) groups. Direct measurements of ABP, respiratory frequency (RF), tidal volume (V T) and ventilation (VE), as well as hypercapnia (7% CO2) and hypoxia (7% O2) evoked respiratory responses were recorded from the awake male offspring at the 30th and 90th days of life. Blood samples were collected for the analyses of protein, creatinine and urea concentrations. The LP offspring had impaired body weight and length throughout the experiment. At 30 d of age, the LP rats showed a reduction in the concentrations of total serum protein (approximately 24%). ABP in the LP rats was similar to that in the NP rats at 30 d of age, but it was 20% higher at 90 d of age. With respect to ventilatory parameters, the LP rats showed enhanced RF (approximately 34%) and VE (approximately 34%) at 30 d of age, which was associated with increased ventilatory responses to hypercapnia (approximately 21% in VE) and hypoxia (approximately 82% in VE). At 90 d of age, the VE values and CO2/O2 chemosensitivity of the LP rats were restored to the control range, but the RF values remained elevated. The present data show that a perinatal LP diet alters respiratory rhythm and O2/CO2 chemosensitivity at early ages, which may be a predisposing factor for increased ABP at adulthood.