Cerebrovascular complications and increased risk of encephalopathies are characteristic of preeclampsia and contribute to 40% of preeclampsia/ eclampsia related deaths. Circulating tumor necrosis factor α (TNFα) is elevated in preeclamptic women and infusion of TNFα into pregnant rats mimics characteristics of preeclampsia. While this suggests that TNFα has a mechanistic role to promote preeclampsia, the impact of TNFα on the cerebral vasculature during pregnancy remains unclear. We tested the hypothesis that TNFα contributes to cerebrovascular abnormalities during placental ischemia by first infusing TNFα in pregnant rats (200 ng/day i.p, from gestational day 14 to 19), at levels to mimic those reported in preeclamptic women. TNFα increased mean arterial pressure (MAP, p<0.05) and brain water content in the anterior cerebrum (p<0.05), however, TNFα infusion had no effect on blood-brain barrier (BBB) permeability in the anterior cerebrum or posterior cerebrum. We then assessed the role of endogenous TNFα in mediating these abnormalities in a model of placental ischemia induced by reducing uterine perfusion pressure followed by treatment with the soluble TNFα receptor (etanercept, 0.8 mg/kg, sc.) on gestational day 18. Etanercept reduced placental ischemia-mediated increases in MAP, anterior brain water content (p<0.05), and BBB permeability (202±44% in placental ischemic rats to 101±28% of normal pregnant rats). Our results indicate that TNFα mechanistically contributes to cerebral edema by increasing BBB permeability and is an underlying factor in the development of cerebrovascular abnormalities associated with preeclampsia complicated by placental ischemia.