HMG-CoA reductase inhibitors (statins) are widely used for secondary prevention of cardiovascular disease and increasing evidence indicates benefits from primary prevention in risk groups. Chronic statin treatment from weaning has been shown to attenuate endothelial dysfunction in adult rats in a model of cardiovascular disease (Torrens et al. 2009) and evidence suggests that early targeted interventions can have long term benefits in this same model (Sherman and Langley-Evans 2000;Vickers et al. 2005). It was hypothesised that early age acute statin treatment would also improve the cardiovascular function in later life in a rat model of developmentally induced cardiovascular disease. Pregnant Wistar rat dams were fed either 18% protein, control (C) or 9% protein restricted (PR) diet throughout pregnancy and were returned to standard chow on delivery. The pups were divided into controls and those receiving atorvastatin, 10mg/kg, (S) for two weeks from weaning at 3 weeks. This gave four experimental groups: control (C), control + statin (CS), protein restricted (PR) and protein restricted + statin (PRS). At 16 weeks blood pressure was assessed with non-invasive tail-cuff plethysmography and vascular reactivity of the mesenteric arteries (MA) was measured ex vivo by wire myography. The differences were assessed with one-way ANOVA and results are expressed as mean±SEM. Significance was assumed at p≤0.05. Increased constriction to PE was observed in PRS groups in both males (C, 4.12±0.16 mN/mm, n=6; CS, 4.57±0.16 mN/mm, n=6; PR, 4.66±0.29 mN/mm, n=5; PRS, 5.27±0.21 mN/mm, n=5; p<0.01) and females (C, 3.22±0.26 mN/mm, n=5; CS, 4.17±0.23 mN/mm, n=6; PR, 3.82±0.40 mN/mm, n=5; PRS, 4.71±0.24 mN/mm, n=6; p<0.01). In female MA increased constriction to endothelin was also shown in the PRS group (C, 3.27±0.56 mN/mm, n=4; CS, 4.43±0.36 mN/mm, n=5; PR, 3.44±0.62 mN/mm, n=4; PRS, 6.20±0.89 mN/mm, n=5; p<0.01). No differences were seen in systolic or diastolic blood pressure or heart rate between the groups. These data show increased constriction in the statin treated PR offspring in adulthood. As data during statin treatment at 5 weeks indicated reduced constriction, the detrimental effects are attributed to statin withdrawal and subsequent rebound. The PR offspring appear to be more susceptible to this as no increase in constriction was observed in the control MA. Investigation into the mechanisms is ongoing.