title: 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.
authors.affiliation: Department of Physiology and Biophysics, Women's Health Research Center, Center for Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
authors.forename: Barbara T
authors.initials: BT
authors.lastname: Alexander
authors.forename: John Henry
authors.initials: JH
authors.lastname: Dasinger
authors.forename: Suttira
authors.initials: S
authors.lastname: Intapad
mesh_terms: D000818:Animals; D002318:Cardiovascular Diseases / Q000196:embryology* / Q000503:physiopathology*; D047109:Fetal Development; D005317:Fetal Growth Retardation / Q000503:physiopathology*; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D009024:Morphogenesis