Rook, William (2011)
Ph.D. thesis, University of Birmingham.
A common consequence of the complications of pregnancy, such as preeclampsia, is reduced supply of nutrients, including oxygen, to the developing fetus. The consequences for the offspring are wide ranging, but include increased risk of cardiovascular disease. However, the mechanisms by which this occurs are poorly understood. Using a rodent model, this study has examined the regulation of blood vessels, particularly those supplying skeletal muscle, by local, endothelially-derived factors, and by the sympathetic nervous system, in adult rat offspring following chronic hypoxia in utero.
The key findings include evidence that there are chronically high levels of oxidative stress in the skeletal muscle vasculature of the offspring. Further, the density of, and the activity in the sympathetic neurones supplying skeletal muscle blood vessels is markedly increased following chronic hypoxia in utero, but the vascular sensitivity to stimulation of these neurones is reduced. Following chronic hypoxia in utero, as the rats approached middle age, they became hypertensive relative to normal rats. Thus, the present study has offered some mechanistic insight, which adds to a growing body of literature, and which may help to explain why babies born of sub-optimal pregnancies are at higher risk of developing cardiovascular disease later in life.
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