Low birth-weight is now known to be associated with increased rates of hypertension in later life. The renin-angiotensin system (RAS) is mainly involved in the regulation of blood pressure. In animal models, alterations of RAS induced by fetal insults such as gestational protein restriction and placental insufficiency may serve as a potential mechanism critical to the fetal programming of hypertension. Blockade of RAS during the nephrogenic period in rats leads to a marked reduction in nephron numbers as well as low birth-weight. The renal RAS suppression during a critical window of nephrogenesis may be a key component in this programming cascade. This article summarizes the potential mechanisms involved in fetal programming of RAS critical to the development of adult hypertension.