Reactive oxygen species (ROS) play a key role in the modulation of vascular tone in physiological and pathological conditions. Pre-eclampsia is associated with raised placental vascular resistance and increased superoxide (O₂^–) (1, 2). Hydrogen peroxide (H₂O₂) is a vasoactive ROS, generated spontaneously and enzymatically from (O₂^–), which may be involved in the regulation of vascular reactivity in the feto- and uteroplacental circulations in normal and complicated pregnancy. Here, we aimed to determine the effects of H₂O₂ on normal chorionic plate and myometrial arterial tone. Normal term placentas (N=13) were collected within 30min of delivery. Myometrial biopsies (N=4) were obtained immediately following hysterectomy in pre-menopausal women with no medical complications. Chorionic plate arteries (n=20, N=5 placentas) and myometrial arteries (N=4) were dissected, mounted onto a wire myograph, and normalized at 0.9 of L_5.1kPa (~20mmHg) and 0.9 of L_13.3kPa (~45mmHg), respectively. The vessels were equilibrated at 37°C for 20 min and gassed at 5% O₂/5% CO₂ (chorionic plate arteries) or 5% CO₂/balance air (myometrial arteries). Preconstricted chorionic plate and myometrial arteries (U46619 thromboxane A₂ mimetic; EC₈₀) were exposed to H₂O₂ (10^-5M) for 10 min and responses compared to time matched controls. In separate experiments, chorionic plate arteries were exposed to H₂O₂ (10^-4M) for 30 min in the presence (n=6, N=3 placentas) and absence (n=16, N=8) of catalase (500U/ml; H₂O₂ scavenger) and responses compared to those of time matched controls (n=10, N=5). H₂O₂ (10^-5M) induced significantly greater relaxation of preconstricted myometrial arteries than of time-matched controls (treatment vs. controls; maximum relaxation to 27±8% vs. 90±8% of U46619 EC₈₀ contraction, mean+SEM, p<0.05 Mann-Whitney U test). In contrast, H₂O₂ (10^-5M) had no effect on U46619 induced tone in chorionic plate arteries. However, chorionic plate arteries exposed to H₂O₂ (10^-4M) constricted transiently (treatment vs. controls; peak increase in baseline tension at 3.2±0.2 mins, 3.8±0.7kPa vs. 0.5±0.4kPa, p<0.05, Mann-Whitney U test). The H₂O₂-induced constriction in chorionic plate arteries was completely inhibited by catalase. Our data reveal differences in human fetoplacental and non-pregnant uteroplacental small artery responses to H₂O₂. The relaxation of myometrial arteries with 10^-5M H₂O₂ is consistent with observations in several systemic vascular beds and may be mediated by the endothelium (3). In contrast, the transient chorionic plate arterial constriction at 10^-4M H₂O₂, a pathophysiologically relevant concentration (4) is probably a direct effect on vascular smooth muscle. We suggest that in pregnancy complications such as pre-eclampsia, excess H₂O₂ could contribute to raised fetoplacental vascular resistance.