A suboptimal intrauterine environment has a number of deleterious effects on fetal development and postpartum health outcomes. Epidemiological studies on several human populations have linked socioeconomic status and low birth weight to an increased incidence of diseases such as hypertension, diabetes, obesity and cardiovascular disease. A growing number of experimental studies in a variety of animal models demonstrate that maternal stressors, such as nutrition and reduced uterine perfusion, affect the intrauterine milieu and result in increased blood pressure in offspring. Several mechanisms appear to contribute to hypertension, including vascular dysfunction and increased peripheral resistance, altered cardio-renal structure and alterations in cardio-renal function. Although many studies have characterized models of developmentally generated hypertension, few have begun to seek therapeutic modalities to ameliorate its incidence. This review discusses recent work that refines hypotheses linking a suboptimal intrauterine environment to cardiovascular and renal phenotypes that have increased susceptibility to cardiovascular disease and hypertension.
Bibliographical noteFunding Information:
The authors recognize the work of Peter Nathanielsz (Center for Pregnancy and Newborn Research) and Stephen Ford (Center for the Study of Fetal Programming). The authors’ work has been supported in part by National Institutes of Health HD21350 and HL65399 (UT), BRIN 1P20RR 16474–01 (UW).
- Blood pressure
- Nephron number
- Vascular dysfunction