Maternal low-protein diet induces changes in the cardiovascular autonomic modulation in male rat offspring

Serotonin modulation in neonatal age does not impair cardiovascular physiology in adult female rats: Hemodynamics and oxidative stress analysis

“…In the second group, this sequence was reversed; the animals were initially administered propranolol and then methylatropine. After each sequence, the intrinsic HR (iHR) was calculated [21,22].…”

Maternal Protein Restriction Increases Respiratory and Sympathetic Activities and Sensitizes Peripheral Chemoreflex in Male Rat Offspring

“…The offspring of rat dams subjected to a maternal low-protein (LP) 10 diet is a model that is often used to study the mechanisms of maternal undernutrition-related hypertension (6)(7)(8), which has been suggested to be associated with changes in the functioning of the sympathetic nervous system (9,10). However, there is no direct evidence demonstrating that sympathetic vasoconstrictor tonus is elevated in rats subjected to a perinatal LP diet.…”

Developmental Origins of Cardiometabolic Diseases: Role of the Maternal Diet

“…Maternal low-protein diet model during both gestation and lactation is one of the most extensively studied animal models of phenotypic plasticity (Ozanne and Hales, 2004; Costa-Silva et al, 2009; Falcão-Tebas et al, 2012; Fidalgo et al, 2013; de Brito Alves et al, 2014; Barros et al, 2015). Feeding a low-protein diet (8% protein) during gestation and lactation is associated with growth restriction, asymmetric reduction in organ growth, elevated systolic blood pressure, dyslipidemia, and increased fasting plasma insulin concentrations in the most of studies in rodents (Ozanne and Hales, 2004; Costa-Silva et al, 2009; Falcão-Tebas et al, 2012; Fidalgo et al, 2013; Leandro et al, 2012; de Brito Alves et al, 2014, 2016; Ferreira et al, 2015; Paulino-Silva and Costa-Silva, 2016).…”

“…Although, the relationship between maternal protein restriction, sympathetic overactivity and hypertension have been suggested (Johansson et al, 2007; Franco et al, 2008; Barros et al, 2015), few studies have described the physiological dysfunctions responsible for producing these effects. Nowadays, it is well accepted that perinatal protein malnutrition raise risks of hypertension by mechanisms that include abnormal vascular function (Franco Mdo et al, 2002; Brawley et al, 2003; Franco et al, 2008), altered nephron morphology and function, and stimulation of the renin-angiotensin system (RAS) (Nuyt and Alexander, 2009; Siddique et al, 2014).…”

“…Nowadays, it is well accepted that perinatal protein malnutrition raise risks of hypertension by mechanisms that include abnormal vascular function (Franco Mdo et al, 2002; Brawley et al, 2003; Franco et al, 2008), altered nephron morphology and function, and stimulation of the renin-angiotensin system (RAS) (Nuyt and Alexander, 2009; Siddique et al, 2014). Recently, studies have highlighted contribution of the sympathetic overactivity associated to enhanced respiratory rhythm and O 2 /CO 2 sensitivity on the development of the maternal low-protein diet-induced hypertension by mechanisms independent of the baroreflex function (Chen et al, 2010; Barros et al, 2015; Costa-Silva et al, 2015; de Brito Alves et al, 2015; Paulino-Silva and Costa-Silva, 2016). Offspring from dams subjected to perinatal protein restriction had relevant short-term effects on the carotid body (CB) sensitivity and respiratory control.…”