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The Developmental Origins of Health and Disease (DOHaD) hypothesis proposes that alterations in fetal nutrition results in developmental adaptations that permane.vtly change structure, physiology and metabolism ofthe offspring to enable survival. These adaptations during early development may determine an individual's susceptibility to a variety of health problems inCluding cardiovascular (CV) disease and related disorders in adult life. It has been proposed that this association may result from impaired prenatal kidney growth and lower nephron endowment at birth induced by suboptimal in utero nutrition. However, the effects of maternal nutrient restriction on fetal kidney development have not been investigated as yet. The aim 0 f this thesis was to investigate if maternal nutrition restriction during gestation results in altered renal or CV development. In the first study ewes received either 100% (C) or 50% (R) oftotal nutrient requirements for the first 31 days of gestation (dGA), and 100% requirements thereafter. In the second study ewes received either 100% (C) of total nutrient requirements throughout gestation, 40% (E) from 1-31 dGA or 50% (L) from 104 dGA onwards, at all other times ewes were fed 100% requirements. In late gestation, fetuses were surgically instrumented and basal CVand renal parameters, and responses to a number ofstimuli were measured. , The first study found that a 50% maternal nutrient restriction did not alter fetal body or organ weights, kidney biometry, basal CV function or baroreflex during late gestation. 50% maternal nutrient restriction had no effect on fetal renin angiotensin system (RAS) in terms of CV or renal response to frusemide. However, the responsiveness to Angiotensin II (Ang In was blunted in the maternal restricted fetuses. The second study found that neither a more severe peri-implantation nor a late gestation maternal nutrient restriction altered any of the fetal parameters measured in the first study. Maternal nutrient restriction did not alter fetal nephron number in late gestation. There was no difference between the groups in the overall CV response to hypoxia. These findings suggest that poor in utero nutrition does not alter renal development and function, basal CV control, baroreflex or chemoreflex in fetal life. Peri-implantation restriction blunted the fetal mean arterial pressure response to Ang II, dependent on intensity of challenge, which may ipdicate altered Ang II receptors populations in the peripheral vasculature. In conclusion reduced maternal nutrition during peri-implantation and late gestation, periods previously implicated as critical periods ofdevelopment, appear to have no effect on fetal renal development.