The factors accounting for the pathological maintenance of a high pulmonary vascular (PV) resistance postnatally remain elusive, but neonatal stressors may play a role in this process. Cross fostering in the immediate neonatal period is associated with adult-onset vascular and behavioral changes likely triggered by early-in-life stressors. Hypothesizing that fostering newborn rats induces long lasting PV changes, we evaluated them at 14 days of age during adulthood, and compared the findings with animals raised by their biological mothers. Fostering resulted in reduced maternal-pup contact time, when compared with control newborns. At two weeks of age, fostered rats exhibited reduced pulmonary arterial endothelium-dependent relaxation secondary to downregulation of tissue endothelial nitric oxide synthase (eNOS) expression and tetrahydrobiopterin deficiency-induced uncoupling. These changes were associated with neonatal-onset increased angiotensin II AT₁ receptor expression, PV remodeling and right ventricular hypertrophy that persisted into adulthood. The pulmonary arteries of adult fostered rats exhibited a higher contraction dose-response to angiotensin II and thromboxane A₂; the latter of which was abrogated by the oxidant scavenger tempol, In conclusion, fostering-induced neonatal stress induces long-standing PV changes modulated via the renin-angiotensin system.