Is Maternal Blood Pressure the Key to Vascular Dysfunction in Preterm Offspring With Elevated Blood Pressure?

Abstract

An inverse association between birth weight and systolic blood pressure was first noted by Barker et al.1 Since then experimental studies have not only substantiated this finding but also provided insight into the potential mechanisms by which adverse influences during critical periods of fetal life lead to increased blood pressure and cardiovascular risk.2 Recent studies indicate that early postnatal influences may also greatly impact cardiovascular risk in the adult,3 suggesting that the critical window of programming extends beyond the prenatal period to early postnatal life. Although influences in early life as determinants of cardiovascular risk are widely accepted, the specific influence of gestational age4 has only recently been acknowledged. Moreover, the mechanism(s) that contribute to high blood pressure in preterm infants, notably the potential role of maternal blood pressure status, has not yet been explored. The original studies by Barker et al1 investigated blood pressure as a link between the intrauterine environment and later cardiovascular risk. The noted inverse relationship between birth weight and blood pressure was not associated with gestational age,1 suggesting that poor fetal growth, not preterm birth, was the major factor contributing to high blood pressure in low birth weight offspring. In this issue of Hypertension , Lazdam et al5 demonstrate that preterm birth, per se, is also a critical influence on later cardiovascular risk. Importantly, the authors also provide evidence that one mechanism by which preterm birth leads to high blood pressure occurs through programmed changes in vascular phenotype that appear to be influenced by maternal blood pressure during …