These findings provide new insights: 1) AII plays a vital role in the maintenance of vascular tension in the placenta, similar to the role of catecholamines in non-placental vessels; 2) AII-mediated physiological function in placental vessels is injured in preeclampsia; 3) the reduced AII-mediated placental vasoconstrictions may cause compensatory responses, resulting in an increase in AII and ACE in the maternal-placental circulation that may induce hypertension in preeclampsia. The gene discussed is ACE; the disease is preeclampsia.