Fetal programming of blood pressure in a transgenic mouse model of altered intrauterine environment

摘要

Key points class="unordered" style="list-style-type:disc" id="tjp7466-list-0001">Nitric oxide is essential in the vascular adaptation to pregnancy, as knockout mice lacking nitric oxide synthase (NOS3) have abnormal utero‐placental perfusion, hypertension and growth restriction.We previously showed with ex vivo studies on transgenic animals lacking NOS3 that adverse intrauterine environment alters fetal programming of vascular reactivity in adult offspring.The current research shows that altered vascular reactivity correlates with higher blood pressure in vivo.Our data suggest that higher blood pressure depends on both genetic background (NOS3 deficiency) and uterine environment, becomes more evident with age (> 7 postnatal weeks), activity and stress, is gender specific (preponderant among males), and can be affected by the sleep–awake cycle. In utero or early postnatal life (< 7 weeks), before onset of hypertension, may represent a potential window for intervention to prevent future cardiovascular disorders.