Inappropriate nutrition during gestation can result in increased risk of diseases such as hypertension in the adult. In our rat model, the possibility that the kidney may play an important role is given credence by the fact that the pups born to Fe deficient mothers, as well as developing hypertension, have smaller kidneys at birth (Gambling et al., 2003; Gambling et al., 2004). In order to test whether the two phenomena are linked, we have examined the expression of genes involved in kidney development and function, specifically vasculogenesis/angiogenesis, apoptosis and cell proliferation. Female Rowett Hooded Lister rats were fed diets with 2 different Fe contents (50 mg Fe/kg and 7.5 mg Fe/kg diet) before and during pregnancy. The dams were killed by exsanguination under terminal anaesthesia at either day 21.5 (D21)of gestation or within 12 hours of giving birth. Fetuses were delivered by caesarean section and killed by a schedule 1 method. Neonates were killed within 12 hours of birth by decapitation. Fetal and neonatal kidneys were collected and processed for mRNA extraction. All experiments were approved by Home office and carried out according to UK Animals (Scientific Procedure) Act, 1986. Using quantitative real time RT-PCR and SYBR Green, we found no difference in gene expression of the markers of vasculogenesis, angiopoietin 1 and 2, vascular endothelial growth factor A and C or haeme oxygenase 1 and 2. Markers of apoptosis, Bcl2 and Bax, showed no differences in expression in either fetal or neonatal kidneys. Cell proliferation markers, p21 and p27, also were not significantly different between the two dietary groups or either time point. In contrast, at D21, renin gene expression was increased in pups from deficient mothers (relative expression. mRNA/18s mRNA; Fe deficient 43.11 ± 3.9, control 30 ± 2.33, p=0.02). This difference disappeared at birth. Expression of other components of the renin-angiotensin system was not affected by maternal diet either in fetal or neonatal samples. In rats, kidney development continues after birth, but little is known concerning the period where it is most vulnerable to nutritional stress. Changes in expression of renin in our model suggest that there could be a window earlier in kidney organogenesis which is more sensitive to maternal influence. Clearly, this requires further investigation.Acknowledgements: This work is supported by the European Union (EARNEST) and Scottish Executive Environment and Rural Affairs Dept (SEERAD).Reference 1 : Gambling, L, Andersen, HS, Czopek, A, Wojciak, R, Krejpcio, Z & McArdle, HJ (2004). Effect of timing of iron supplementation on maternal and neonatal growth and iron status of iron-deficient pregnant rats. J. Physiol. 561, 195-203. Reference 2 : Gambling, L, Dunford, S, Wallace, DI, Zuur, G, Solanky, N, Srai, SKS & McArdle, HJ (2003). Iron deficiency during pregnancy affects post-natal blood pressure in the rat. J. Physiol. 552, 603-610.