Fetal Programming and Cardiovascular Pathology

Abstract

Low birth weight serves as a crude proxy for impaired growth during fetal life and indicates a failure for the fetus to achieve its full growth potential. Low birth weight can occur in response to numerous etiologies that include complications during pregnancy, poor prenatal care, parental smoking, maternal alcohol consumption or stress. Numerous epidemiological and experimental studies demonstrate that birth weight is inversely associated with blood pressure and coronary heart disease. Sex and age impact the developmental programming of hypertension. In addition, impaired growth during fetal life also programs enhanced vulnerability to a secondary insult. Macrosomia, which occurs in response to maternal obesity, diabetes and excessive weight gain during gestation, is also associated with increased cardiovascular risk. Yet, the exact mechanisms that permanently change the structure, physiology and endocrine health of an individual across their lifespan following altered growth during fetal life are not entirely clear. Transmission of increased risk from one generation to the next in the absence of an additional prenatal insult indicates an important role for epigenetic processes. Experimental studies also indicate that the sympathetic nervous system, the renin angiotensin system, increased production of oxidative stress and increased endothelin play an important role in the developmental programming of blood pressure in later life. Thus, this review will highlight how adverse influences during fetal life and early development program an increased risk for cardiovascular disease including high blood pressure and provide an overview of the underlying mechanisms that contribute to the fetal origins of cardiovascular pathology.

Developmental cigarette smoke exposure II: Hepatic proteome profiles in 6 month old adult offspring

“…Interestingly, more recent studies have established compelling linkages between pre-/perinatal exposures to cigarette smoke and an increased risk of offspring obesity and metabolic disease [17–25]. While the ability of prenatal and early-life environmental exposures such as cigarette smoke to elicit developmental programming and long-lived alterations in adult health/disease risk has been well documented [1, 4, 26–31], the precise biological mechanisms by which such exposures dysregulate the development, function, and adaptability of the organism’s key metabolic regulatory tissues/organs are still largely unknown.…”

Prenatal glucocorticoid exposure programs adrenal PNMT expression and adult hypertension

“…Examples of such stressors include maternal nutrient restriction, hypoxia, physical trauma, as well as exposure to alcohol and nicotine. There is a large and growing body of evidence linking an adverse prenatal environment to the fetal programming of cardiovascular disease in adult life (Vehaskari & Woods 2005, Cottrell & Seckl 2009, Alexander et al 2015. Low birth weight and developmental programming of hypertension has been correlated with impaired kidney development and dysregulated renin-angiotensinaldosterone system (Baum 2010, Goyal et al 2010, impaired vascular structure and function (Pladys & Sennlaub 2005, Ligi et al 2010, as well as altered activity of the hypothalamic-pituitary-adrenal (HPA) (Bouret 2009, Boyne et al 2009, and the sympatho-adrenal (SA) axes (Young 2002, Johansson et al 2007.…”

La psychocardiologie : une nouvelle spécialité

“…Il faut également mentionner les effets génétiques du SPS.D ansu ne réaction de défense et de survie de l'espèce,l es tress aigu et chronique peut provoquer des modifications épigénétiques chez les foetus de femmes stressées [42]. Ces modifications épigénétiques entraîneront pour les individus issus de telles grossesses, une hyper réactivité au stress, une tendance à l'anxiété généraliséee tàla dépression en perturbant le transport de la sérotonine.…”