The vasoactive effects of oxidative stress induced by hydrogen peroxide (H₂O₂) on human umbilical artery strips as well as the possible mechanisms involved are studied. Contraction responses to cumulative H₂O₂ (10^–7 M-3 × 10^–2 M) in endothelium intact and denuded umbilical arteries and responses to cumulative H₂O₂ after incubation with L-NAME (10^–4 M) (n = 8), indomethacin (10^–5 M) (n = 8) and verapamil (10^–6) (n = 8) were recorded. Responses elicited with cumulative H₂O₂ in Ca²⁺ free extracellular medium and the responses to cumulative Ca²⁺ (10^–4 M-2 × 10^–3 M) after H₂O₂ (10^–3 M) induced contraction were also studied. The Emax for each experiment was calculated. p <0.05 was considered as significant. H₂O₂ elicited contraction was greater in endothelium denuded artery strips compared to endothelium intact strips (p < 0.05). Compared to control, incubation with L-NAME significantly augmented (p < 0.05), while verapamil and indomethacin inhibited the contractions elicited by cumulative H₂O₂ (p < 0.05). Ca²⁺ free extracellular medium caused decreases in cumulative H₂O₂ elicited contractions and cumulative Ca²⁺ caused concentration dependent increases in the contraction caused by a single bolus of H₂O₂ (p < 0.05). Exposure to H₂O₂ causes concentration-dependent constriction in human umbilical arteries. The presence of the endothelium and NOS enzyme activation influences the H₂O₂ responses. Removal of the endothelium increases the H₂O₂ elicited contractions more than incubation with L-NAME suggesting beside NO, other endothelial vasodilators are also involved in vascular tonus of the umbilical arteries. Both intracellular and extracellular Ca²⁺ ions and constrictor cyclooxygenase metabolites play a role in the contractile responses elicited by H₂O₂ in human umbilical arteries.