Intrauterine Programming and Postnatal Hypertension

The adult phenotype is known to be dependent on environmental signals operating during intrauterine development. This study reviews the effect and the mechanisms of intrauterine programming-induced hypertension. Low birth weight impairs endothelial dependent and non-endothelial dependent vasodilatation by decreasing endothelial NO synthase (eNOs) and eNOs activity, increasing pressor response to angiotensin II, increasing apoptosis in fetal heart and increasing sympathoadrenergic activity. It also leads to permanent structural alterations of the kidneys with a high tendency to cardiorenal disease.