We have shown that chronic hypoxia in-utero (pregnant dams breathing 12% O₂ during the second half of pregnancy) may lead to a reduction in nitric oxide (NO) bioavailability in the vasculature of the adult offspring¹. Superoxide anions (O₂^–) are implicated in reducing NO bioavailability by directly reacting with NO to produce peroxynitrite. Superoxide dismutase (SOD) catalyses the dismuting of O₂^– into H₂O₂ and O₂, thus protecting NO bioavailability. In light of this, we have now investigated the role of SOD in skeletal muscle vasculature in CHU offspring. Under anaesthesia (Alfaxan; 3-6ml hr^-1kg^-1i.v.), we recorded arterial blood pressure (ABP) and femoral blood flow (FBF) in 9-10 week old normal (N, n=12) rats and in age-matched CHU (CHU, n=8) offspring. Femoral vascular conductance (FVC) was calculated (FBF/ABP) and integrated FVC (IntFVC) used to give an indication of vascular tone. Variables were recorded during air breathing and during 10min periods of acute systemic hypoxia (breathing 8% O2) before and during infusion of the cell permeant SOD inhibitor Diethyldithiocarbamate trihydrate (DETC; 5mg^-1.kg^-1.min^-1 i.v.) Baseline ABP was similar in both groups (N:136±3, CHU:143±5mmHg) as was baseline IntFVC (N:7.9±1.1, CHU:6.3±1.1 CU) resulting in similar FBF (N:5.4±0.6, CHU:4.6±0.9ml^-1min^-1kg^-1). As previously shown, responses to acute hypoxia were similar in both N and CHU with both showing a fall in ABP, an increase in IntFVC which maintained FBF at control levels. DETC caused a small increase in ABP, although not statistically significant (N:137±3, CHU:149±3 mmHg). DETC also caused a significant reduction in IntFVC (N:0.6±0.7, CHU:1.8±0.6) in CHU, but not N rats, which was mirrored by changes in FBF (N:-0.2±0.4, CHU:-1.1±0.3). Inducing acute hypoxia during DETC infusion caused ABP to fall. However, it remained at a level higher than under control conditions in both N and CHU (N:79±5, CHU:77±3). There was no difference in the magnitude of muscle vasodilatation induced by hypoxia as indicated by a similar increase in IntFVC. SOD normally dismutes O₂^– into the vasodilator H₂O₂, therefore, SOD antagonism results in the build up of (O₂^– and induces vasoconstriction. The reduction in FVC in air breathing CHU rats during DETC administration suggests increased basal production of O₂^– anions that is not apparent in N rats. It is possible that this O₂^– production is through uncoupling of nitric oxide synthase². However, in keeping with our previous findings with shorter periods of hypoxia¹, the acute response to hypoxia and is similar in both N and CHU rats. Further, there is no apparent difference during DETC infusion suggesting the increased O₂^– production in CHU rats is only evident during air breathing. Preliminary findings in the carotid artery suggest there may also be differences in other vascular beds, warranting further work.