Maternal protein restriction (PR) in rats induces vascular dysfunction and though this can be ameliorated by chronic statin treatment, statin treatment and withdrawal in adolescent rats leads to a sustained increase in mesenteric artery constriction. In adult rats increase in constriction after statin withdrawal has been shown to be transient and RhoA pathway has been implicated as the mechanism. RhoA promotes constriction by activating Rho kinases (ROCK) which inhibit myosin light chain phosphatase. Statins inhibit RhoA activity but increase RhoA mRNA levels which remain elevated briefly after statin withdrawal contributing to increased RhoA activity. In this study the mRNA levels of RhoA pathway genes were investigated in the control and PR rat offspring mesenteric arteries where withdrawal of early age statin treatment lead to sustained increase in constriction. Male and female Wistar rat offspring of dams fed 18 % protein (control) or 9 % protein restricted (PR) diet during pregnancy were given atorvastatin (10mg/kg) in drinking water from 3-5 weeks. This gave four experimental groups; control, no statin (CS: n=6 males, n=5 females), control, statin (CS: n=6 both), PR diet, no statin (PR: n=5 males, n=4 females) and PR diet, statin (PRS: n=5 both). At 16 weeks the animals were euthanised with CO2 inhalation and cervical dislocation. Segments of mesenteric arteries were frozen in liquid nitrogen. RNA extraction was carried out in Trizol and RNA was reverse transcribed into cDNA. Real time PCR was carried out with FAM/TAMRA primers and probes and gene expression was normalised against β-actin which was chosen as a stable housekeeping gene after geNorm analysis. mRNA levels of RhoA, ROCK 1 and ROCK 2 were investigated. The differences were assessed with two-way ANOVA. Results are presented as mean±SEM. Significance was accepted at p<0.05. No significant differences were seen in mRNA levels of RhoA in the males (p>0.05) but in the females statin treatment increased RhoA mRNA expression irrespective of maternal diet (RhoA/b-actin: C 0.63±0.06; CS 0.86±0.10; PR 0.53±0.05; PRS 0.70±0.07; p<0.05 for statin effect; p>0.05 for maternal diet effect and interaction). Statin treatment increased ROCK 1 mRNA levels in the male offspring irrespective of maternal diet (ROCK1/β-actin: C 0.55±0.06; CS 0.93±0.11; PR 0.70±0.14; PRS 0.90±0.17; p<0.05 for statin effect; p>0.05 for maternal diet effect and interaction) but no significant differences were seen in the females (p>0.05). No significant differences were seen in the ROCK 2 mRNA levels in either males or females (p>0.05). These data indicate that sustained upregulation of gene expression of RhoA pathway genes in the mesenteric arteries could contribute to the long term increase in constriction observed after withdrawal of early age statin treatment in C and PR offspring.