<i>In vivo</i> and <i>in vitro</i> studies on numerous types of blood vessels obtained from a variety of vascular beds and species have demonstrated that oxygen free radicals (OFRs) can evoke both vasodilation and vasoconstriction. Specific OFRs have been shown to elicit different and often times opposite effects on vascular smooth muscle. Therefore, this thesis attempts to define the vascular actions and mechanism of oxygen free radicals (OFRs) [superoxide anion (O₂^-), hydrogen peroxide (HO₂) and hydroxyl radical (OH)] on isolated rabbit aorta. This thesis will examine the role of OH in Ach- and nitroglycerin (NTG)-induced relaxation of isolated rabbit aorta. Superoxide anions generated by xanthine (X) plus xanthine oxidase (XO) produced concentration-dependent contractions of isolated rabbit aorta. The contractile response to O₂^- was completely abolished in preparations denuded of endothellum or pretreated with superoxide dismutase (SOD), a scavenger of O₂^-. The contractile response was reduced by indomethacin (I), a cyclooxygenase inhibitor. These results suggest that O₂^- mediated by vasoconstrictor arachidonic acid metabolites. Hydrogen peroxide generated by glucose and glucose oxidase produced contraction (low concentrations) and relaxation followed by contraction (high concentrations) in isolated rabbit aorta. The contractile response was abolished in the presence of catalase, a scavenger of H₂O₂ however the relaxant effect was exaggerated. Indomethacin markedly reduced the H₂O₂-induced contraction. Relaxation was completely prevented by de-endothelialization or pretreatment with N^G-monomethyl-L-arginine (LNMMA), an inhibitor of nitric oxide synthetase. These results suggest that H₂O₂ in large concentrations produces a biphasic response, relaxation followed by contraction. Relaxation is endothelium dependent and is mediated by endothelium-derived relaxing factor (EDRF), nitric oxide (NO). The contractile response is endothelium independent and is mediated by vasoconstrictor arachidonic acid metabolites of smooth muscle. Hydroxyl radicals generated by dihydroxyfumarate (DHF), ferric chloride (FeCl₃) and adenosine diphosphate (ADP) (DHF/FeCl₃-ADP) produced concentration dependent relaxations of NE-precontracted rabbit aorta. Mannitol (Ml) completely inhibited OH-induced relaxation. Relaxation was markedly reduced in aortic rings mechanically denuded of endothelium. The relaxant effect was reduced by an inhibitor of NO synthesis (LNMMA), by an inhibitor of guanylate cyclase (methylene blue), by an inhibitor of cyclooxygenase (indomethacin) and by an inhibitor of an ATP-sensitive K⁺ channel blocker (glyburide). These results indicate that OH produces relaxation that is endothelium-dependent and partially mediated by an endothelium-derived relaxing factor (NO), vasodilatory arachidonic acid metabolites and an ATP-sensitive K⁺ channel. We hypothesized that Ach-induced vascular relaxation is mediated by OH derived from the interaction of NO and O₂^-. To test this hypothesis we investigated the effect of Ach and NTG on NE-precontracted isolated rabbit aortic preparations in the absence or presence of scavengers of O₂^- (SOD), and OH (dimethylthiourea (DMTU) or mannitol or Garlicin). The OFR scavengers (SOD, dimethylthiourea, mannitol, garlicin and histidine) alone or the combination of SOD and DMTU markedly reduced Ach- or NTG-induced relaxation. However, the combination of histidine, (a ¹O₂ scavenger) SOD and DMTU completely abolished Ach-induced relaxation.