Hypertension is a multi-factorial disorder thought to result from both genetic and environmental factors. Numerous epidemiological studies report an association between birth weight and blood pressure. This association is observed in a variety of populations from around the world and is further supported as elevations in blood pressure are also found in low birth weight children Thus, the inverse relationship between birth weight and blood pressure suggests that factors present in the fetal environment which affect fetal growth are responsible for the developmental programming of blood pressure control. Recent experimental studies suggest that developmental programming occurs in response to adverse environmental influences during fetal life resulting in permanent adaptive responses that lead to structural and physiological alterations and the subsequent development of cardiovascular disease and hypertension. Sex differences in response to fetal insult are observed in many animal models of developmental programming with phenotypic outcome linked to the severity of the insult. In general, phenotypic outcome is more severe in male offspring relative to females (1). Although the exact mechanisms that mediate the sexual dimorphism in programmed blood pressure are unclear, experimental studies suggest that sex-specific programming of blood pressure involves a key role for the kidney (1), the renin angiotensin system (2), oxidative stress (3), and sex steroids (4). Whether a sex difference in blood pressure is present in low birth weight men relative to low birth weight women has not been clearly established. However, one study indicates that blood pressure is higher in low birth weight boys relative to low birth weight girls during childhood (5). Other studies indicate that men demonstrate a strong association between birth weight and blood pressure in young adulthood (6), whereas hypertension is not present until age 60 in low birth weight women (7). Thus, these studies suggest that the association between birth weight and blood pressure amplifies with age. Moreover, age may adversely impact the protective role of the female sex on programming of later chronic health. It is well established that aging is a critical mediator of age-related increases in blood pressure. Yet, few experimental studies have examined the impact of aging on sex differences in programmed hypertension. Thus, susceptibility to developmental programming of hypertension is sex-specific. However, age-dependent changes may serve as a secondary influence following fetal insult implicating a need for further studies to investigate the impact and the mechanisms involved in age-dependent increased cardiovascular risk in low birth weight men and women.