The link between being small for gestational age and increased risk of adult cardiovascular disease is well established (1). It has been shown that chronic hypoxia in utero (CHU) and chronic maternal nutrient deficiencies have distinct effects on vascular function (3). However, it is known that both insults can lead to hypertension, although the origin/s of this are not understood. Endothelial dysfunction has been found in mesenteric arteries of rats subjected to CHU (4). However, equally importantly, increased sympathetic nerve density has been shown in femoral arteries of neonatal chicks subjected to CH in the egg (2), suggesting that neurogenic, as well as endothelial factors may contribute to the increased rates of cardiovascular disease seen in the adult animals. To address this, we have compared in vivo recordings from single sympathetic neurones supplying the Spinotrapezius muscle vasculature in 10 week old male Wistar rats subjected to CHU (12% O2 from gestational d11-21) to those made in normal (N) rats. Under anaesthesia (Alfaxan, 3-6mg.kg-1.hr-1 I.V.), an in vivo preparation of the Spinotrapezius muscle was made as described by Marshall (1982, 5). Arterial blood pressure (ABP) and tracheal pressure were recorded via pressure transducers. Nerve recordings were made by applying light suction via a glass microelectrode (~30μm tip) to the surface of an arteriole supplying the spinotrapezius. They were analysed using Spike2 software. Single units were discriminated from multi unit recordings (generally 2-3 units/recording), by using spike shape templates, followed by analysis of principle components. When breathing 21% O2 in N2. mean ABP was similar in N and CHU rats (N: 121±3, CHU: 119±5, mmHg, mean±SEM). 43 single units were discriminated (N: 17 units, N=7, CHU: 26 units, N=6). All units had both cardiac and respiratory rhythm (as assessed by stimulus triggered histogram analysis using the ABP and tracheal pressure traces), confirming they were sympathetic neurones. Mean firing frequency in individual units was similar in N and CHU (0.48±0.09,vs 0.52±0.1, Hz; mean±SEM) These preliminary results suggest that resting sympathetic nerve activity in individual fibres supplying skeletal muscle vasculature is not affected by CHU. However, if there is increased sympathetic nerve density in CHU, the overall sympathetic tone reaching the resistance arterioles may be increased. Work is ongoing to determine the sympathetic nerve density and to compare responses evoked in MSNA by stimuli such as acute hypoxia and baroreceptor challenge in CHU and N rats. These new findings have the potential to make a major contribution to our understanding of how adult cardiovascular disease is programmed during development.