Premature birth is a factor of increased blood pressure in adulthood. Little is known about the physiologic characteristics of the arterial bed in neonates. The aim of this study was to characterize in vivo the arterial compliance in neonates and its maturation profile in very low birth weight (VLBW) premature infants. A group of stable, VLBW premature infants was compared with a control group of near term neonates. The abdominal aortic wall distensibility coefficient (DC) and whole-body arterial compliance (WBAC) were determined using specifically designed noninvasive methods, based on ultrasonic measurements in combination with synchronous, beatto-beat recording of aortic pulse pressure (PP). On the fifth day of life, WBAC and the CD were lower in VLBW premature infants than in controls. Furthermore, WBAC and the DC remained unchanged in VLBW premature infants 7 wk after birth. In conclusion, VLBW premature infants are characterized as early as the fifth day of life by high arterial stiffness, which persists when they reach their theoretical term. It can be speculated that early alteration of arterial elastic properties may pave the way for long-term elevation of arterial pressure in VLBW premature infants. (1) identified a relationship between low birth weight and increased risk of arterial hypertension, carotid arteriosclerosis, and mortality by coronary heart disease or stroke in adulthood. More recently, a relationship has been shown between preterm birth and cardiovascular or metabolic disorders in adult life (2,3). An inverse relationship between adult blood pressure and gestational age has been found in both adult men and women who were born prematurely (4,5). Furthermore, a large epidemiologic study has reported that young male adults born extremely preterm faced an almost twofold increased risk (Ն140 mm Hg) compared with subjects born at term (6). Last, blood pressure, pulse pressure, and vascular resistance have been reported to be increased in preterm girls after puberty (7).Numerous animal studies based on diet restriction during pregnancy, uterine artery ligature, or antenatal exposure to dexamethasone have shown that low birth weight is associated with increased arterial blood pressure in adulthood (8,9). The mechanisms, however, are not fully known. Low birth weight has been shown to be associated with nephron number reduction and increased blood pressure in adulthood (9,10). Moreover, arterial wall structure or properties may be affected, as shown by the relationship between brachial artery flowmediated dilation, endothelium-dependent response, and birth weight (11). Also, an inverse relationship has been observed between pulse wave reflections and birth weight (12). Several authors argue that in fetuses with impaired growth, elastin synthesis in the wall of the aorta and of large arteries may be deficient and may lead to permanent changes in mechanical properties (13,14). Studies aimed at clarifying the relationship between arterial stiffness and low birth weight have led to similar ...