Endothelial Damage and Hypertension
Current research suggests that preeclampsia arises from poor oxygen flow to the placenta due to problems with the development of the placenta. As a result, the diseased placenta then releases factors such as sFlt1 (a protein that causes damage to endothelial and placental cells). Damage to endothelial cells eventually lead to the signs and symptoms of preeclampsia including hypertension, proteinuria, and liver dysfunction. Scientists have recently discovered that sFlt1 interferes with the growth and development of endothelial and placental cells. Animal research involving the injection of sFlt1 into pregnant rats has shown it causes them to develop preeclampsia.
Many women with preeclampsia have higher levels of sFlt1 circulating in their blood than women with normal pregnancies. Although all women with preeclampsia do not have higher levels of sFlt1, it is proposed that other undiscovered factors released from the placenta play a role in the development of preeclampsia.
Elevated pressure within blood vessels and damaged endothelial tissue causes the fluid in the blood vessels to flow into surrounding tissue. This can cause edema (swelling) in the brain, retinas, lungs, liver, and subcutaneous tissues. Edema is one of the central features of preeclampsia.
Hypertension and endothelial damage to capillaries (small blood vessels) in the kidneys cause a breakdown in the kidney's functions. This results in proteins-which are generally retained by the body-being excreted in the urine ( proteinuria ), a symptom of preeclampsia.
The damage to endothelial tissue and the other processes just described lead to low levels of red blood cells (anemia) and low blood platelet levels (leading to impaired blood clotting). Both can cause difficulties during and after labor. Likewise, edema due to preeclampsia can lead to serious complications.