Vazoactive Effects of Oxidative Stress Elicited by Hydrogen Peroxide in the Human Umbilical Artery: An in Vitro Study

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.