Abstract
We have previously shown that the abnormal intrauterine environment in mice lacking the endothelial nitric oxide synthase (NOS3) leads to hypertension and abnormal vascular function in the adult offspring. NOS3, vascular endotelial growth factor receptor-1(VEGF-R1) and tumor necrosis factor-á (TNFá) are known to play a role in utero-placental perfusion, angiogenesis and inflammation. Our objective was to evaluate their involvement in the altered fetal programming of adult vascular function in this transgenic model of utero-placental insufficiency.
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