The placental renin angiotensin system

Intrauterine growth restriction (IUGR) and preeclampsia are major and common complications of human pregnancy. Not only do they represent life threatening events for mothers and babies but they also enhance the susceptibility of the baby to diseases like hypertension, coronary artery disease and diabetes mellitus in adult life. One of the major causes of IUGR and preeclampsia is impaired placentation. Development of the placenta requires a complex interplay between proliferation of trophoblast cells and their invasion of the maternal decidua and maternal spiral arterioles, which they plug so that the early placenta (<12 weeks gestation) normally develops in a hypoxic milieu. The placenta contains its own renin angiotensin system (RAS). Angiotensin II, the end-product of the renin-renin substrate reaction, acting through its type 1 receptor stimulates placental angiogenesis and trophoblast invasion and migration and is involved in placental development. This chapter outlines the expression and localisation of the placental RAS, the role of the placental RAS in placental development and function throughout pregnancy and how disturbances in the placental renin angiotensin system likely contribute to the pathogenesis of PreE and IUGR.