We previously observed that vascular remodeling in response to vascular injury is exaggerated in fetal growth restriction (FGR) mice. We reported that angiotensin II type 2 receptor (AT₂R) stimulation prevented cerebral ischemic damage. The AT₂R is highly expressed in fetal mice. However, the effects of AT₂R on ischemic brain damage in FGR mice is unclear. Therefore, we investigated the roles of AT₂R in brain damage in FGR mice using transgenic mice with overexpressed AT₂R in vascular smooth muscle cell (smAT₂-Tg) mice. Dams (wild-type and smAT₂-Tg mice) were fed an isocaloric diet containing 20% protein (NP) or 8% protein (LP) until delivery. On the day of delivery, all dams were returned to the NP diet. After weaning, offspring were fed the NP diet. When male offspring were 10 weeks of age, cerebral ischemic injury was induced by transient middle cerebral artery occlusion (MCAO). Systolic blood pressure did not differ among all groups at 10 week of age. Ischemic area 48 hours after MCAO in NP mice was smaller in smAT₂-Tg mice. Stroke size in WT-LP mice was significantly larger compared with WT-NP mice. This aggravation of stroke size by LP was weaker in smAT₂-Tg-LP mice. Cerebral blood flow in the whole brain in smAT₂-Tg mice was attenuated compared with that in WT mice at 48 hours after MCAO. These results suggested that AT₂R could enhance the cerebral protective effects in FGR at least in part due to the increase of CBF after ischemia.