vascular smooth muscle until 2 wk postnatal when they are replaced by AT 1 . Thus, the mechanisms whereby ANG II increases MAP after birth are unclear. We examined the effects of ANG II on femoral vascular resistance (FmVR) and blood flow (FmBF) in serial studies of newborn sheep (n ϭ 7) at 7-14 d, 15-21 d, and 22-35 d. Animals had femoral catheters implanted for systemic ANG II infusions and cardiovascular monitoring, and a flow probe was implanted on the contralateral artery proximal to the superficial saphenous artery, which contained a catheter for intra-arterial ANG II infusions. Studies were performed using a range of systemic and intra-arterial ANG II doses. Systemic ANG II increased MAP dose-dependently at all ages (p Ͻ 0.001); however, responses were not age dependent. FmBF rose dose dependently at 7-14 d (p Ͻ 0.001) and was unchanged at older ages. The transition from fetal to newborn life is associated with numerous hemodynamic changes, including alterations in HR, blood pressure, PVR, and the distribution of cardiac output (1-4). The autonomic nervous system and the reninangiotensin system (RAS) are considered important modulators of the cardiovascular changes in the perinatal period. This is supported by evidence of increased circulating levels of catecholamines and ANG II during and after parturition (1, 4 -6). ANG II is the predominant vasoactive agent associated with the RAS and is believed to be an important regulator of blood pressure in fetal, neonatal, and adult sheep (7-9). The effects of ANG II on blood pressure may reflect its direct action on VSM through increases in PVR or on cardiac output by increasing venous return or HR (4, 10 -13). Indirect effects on VSM also may occur through activation of central autonomic nervous system activity or the release of other vasoactive mediators (11, 14 -16).ANG II mediates its actions by binding to specific AT. At least two AT subtypes have been identified, AT 1 and AT 2 , and their expression is developmentally regulated (17)(18)(19). In the adult, the AT 1 is the primary subtype expressed in most tissues, including VSM, and accounts for most biologic actions of ANG II (20,21). However, AT 2 are found in selective adult tissues, e.g. adrenal, myometrium, and uterine arteries from pregnant and nonpregnant women and sheep (9,(21)(22)(23)