Assuntos
Progressão da Doença , Retardo do Crescimento Fetal/fisiopatologia , Hipertensão/prevenção & controle , Retardo do Crescimento Fetal/prevenção & controle , Retardo do Crescimento Fetal/terapia , Humanos , Hipertensão/etiologia , Sistema Renina-Angiotensina , Fatores de Risco , Túnica Íntima/patologia , Rigidez VascularRESUMO
Environmental conditions during perinatal development such as maternal undernutrition, maternal glucocorticoids, placental insufficiency, and maternal sodium overload can program changes in renal Na(+) excretion leading to hypertension. Experimental studies indicate that fetal exposure to an adverse maternal environment may reduce glomerular filtration rate by decreasing the surface area of the glomerular capillaries. Moreover, fetal responses to environmental insults during early life that contribute to the development of hypertension may include increased expression of tubular apical or basolateral membrane Na(+) transporters and increased production of renal superoxide leading to enhanced Na(+) reabsorption. This review will address the role of these potential renal mechanisms in the fetal programming of hypertension in experimental models induced by maternal undernutrition, fetal exposure to glucocorticoids, placental insufficiency, and maternal sodium overload in the rat.
Assuntos
Hipertensão/embriologia , Rim/fisiopatologia , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Animais , Feminino , Taxa de Filtração Glomerular , Glucocorticoides/farmacologia , Humanos , Hipertensão/fisiopatologia , Rim/embriologia , Desnutrição/complicações , Desnutrição/embriologia , Desnutrição/fisiopatologia , Fenômenos Fisiológicos da Nutrição Materna , Insuficiência Placentária/fisiopatologia , Gravidez , Ratos , Sódio na DietaRESUMO
Historically, genetics and life style have been considered the primary underlying causes of hypertension. However, recent epidemiological studies indicating that size at birthis linked to increased cardiovascular risk and hypertension in later life suggest that prenatal influences contribute to the development of hypertension and cardiovascular disease. Confirmatory findings from animal studies demonstrate that prenatal programming occurs in response to an adverse fetal environment and leads to permanent alterations in the structure and pathophysiology of the fetus resulting in the disregulation of blood pressure control andan increased cardiovascular risk in later life. This review will concentrate on the common phenotypic outcomes of prenatal programming and discuss potential mechanisms that mediate these adaptive responses.