Epidemiological studies demonstrate that low birth weight is associated with an increased risk of cardiovascular disease in adult life (Osmond et al., 1993). In the rat, the restriction of dietary protein during gestation leads to raised systolic blood pressure and endothelial dysfunction in the offspring, possibly due to defects in the nitric oxide (NO) pathway (Lamireau et al., 2002; Torrens et al., 2006). Statins (HMG-CoA reductase inhibitors) are used in the management of dyslipidaemia, but have been shown to have other pleiotropic actions, including increasing NO bioavailability and reducing oxidative damage (Davidson et al., 2005). The aim of this study was to assess the effect of statin therapy on endothelial function in offspring of protein restricted dams, in a vascular bed which was predominantly NO dependent. Pregnant Wistar rats were fed a control (C; 18% casein) or protein restricted (PR; 9% casein) diet throughout pregnancy and returned to standard chow postpartum. At weaning a subset of the PR group were given atorvastatin (PRS, 10 mg/kg/day) in the drinking water. At 145 days of age male offspring were sacrificed by CO₂ inhalation and cervical dislocation. To assess vascular function 2 mm aortic segments were mounted in an organ bath. Concentration response curves were conducted to phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP). Responses to ACh were repeated in the presence of L-NAME (100 µM). Data is given as mean ± S.E.M. and differences were assessed by one-way ANOVA with Bonferroni post hoc correction. Significance was accepted at p<0.05. In male aortae the contractile responses to PE were increased in the PRS group compared to all other groups (% max response: C, 138.3 ± 4.0, n= 7; PR, 160.6 ± 5.4, n= 8; PRS, 190.3 ± 12.7, n= 5, p<0.05). Vasodilation to ACh was significantly blunted in both the PR and PRS groups compared to controls (% max response: C, 79.4 ± 3.6, n= 6; PR, 48.9 ± 7.3, n= 8; PRS, 45.5 ± 3.1, n= 5; p<0.05). Incubation with L-NAME completely abolished the ACh response in all groups. No differences were in seen in the response to SNP (p=ns). The data demonstrates that protein restriction during gestation leads to vascular dysfunction in isolated thoracic aorta segments from the male adult offspring. Results show relaxation to ACh is entirely NO dependent and indicates that abnormalities in the NO pathway may be responsible for the attenuated responses in the PR groups. Despite the reported pleiotropic effects of statins, and what we previously have reported in the small mesenteric arteries (Torrens et al., 2007), statin treatment did not restore vascular function in the thoracic aortae of the PR group.