Figure 1. Autoantibodies from women with preeclampsia are functional mimics of Ang II and activate AT₁ receptors on many cell types.

Autoantibody-induced AT₁ receptor activation on cardiac myocytes leads to increased contraction rates. The activation of AT₁ receptors on mesangial cells and trophoblast cells results in increased synthesis and secretion of soluble factors such as interleukin-6 (IL-6), plasminogen activator inhibitor-1 (PAI-1), and soluble fms like tyrosine kinase-1 (sFlt-1, a soluble form of the vascular endothelial growth factor-1 receptor), all of which are elevated in women with preeclampsia. In addition, AT₁-AAs stimulate the synthesis of NADPH oxidase in several cell types, resulting in increased production of reactive oxygen species (ROS) and oxidative damage. Increased production of tissue factor (TF) by vascular smooth muscle cells and monocytes may contribute to hypercoagulation often associated with preeclampsia. We propose that AT₁-AA activate AT₁ receptors on many cell types and in this way contribute to pathophysiological changes associated with preeclampsia.