A new study by researchers at Wake Forest University School of Medicine reveals a key component in the development of preeclampsia in pregnant women, a condition that can result in miscarriage and maternal death.
The study, funded by the National Institutes of Health, appears in the September issue of Endocrinology.
In it, researchers focused on identifying the differences in the uteri of pregnant women with and without preeclampsia and how the mother's tissues vary from the immediately adjacent fetus' tissue in preeclamptic women.
"Preeclampsia is a very serious condition that affects 7 to 10 percent of all pregnancies in the United States," said K. Bridget Brosnihan, Ph.D., the lead investigator for the study and a professor in the Hypertension and Vascular Research Center at the School of Medicine. "It can be devastating to both mother and baby, and currently there is no cure except to deliver the fetus. Our finding brings us one step closer to understanding the condition by getting a picture of what is happening at the maternal and fetal interface."
Preeclampsia is a disorder that occurs only during pregnancy and the postpartum period. It is a rapidly progressive condition that impacts multiple body systems, causing high blood pressure, decreased liver function and, in the most severe cases, affecting the activity of the brain, resulting in seizures. Swelling, sudden weight gain, headaches and changes in vision are among the symptoms; however, some women with rapidly advancing disease report few symptoms.
Left untreated, preeclampsia can lead to serious, even fatal, complications for both mother and baby. The condition contributes significantly to neonatal morbidity and mortality and is the second leading cause of maternal death. By conservative estimates, preeclampsia and other hypertensive disorders during pregnancy are responsible for 76,000 maternal and 500,000 infant deaths each year, according to the Preeclampsia Foundation.
Despite numerous research studies, the specific causes of preeclampsia remain a mystery. One possible pathway that has been identified is the renin-angiotensin system (RAS), which regulates blood pressure and fluid retention.
The RAS, when operating normally, forms a hormone called angiotensin II, a potent vasoconstrictor that binds to angiotensin II receptors throughout the body, including in the maternal uterine "bed" and the fetal placenta, and causes the muscular walls of blood vessels to contract, narrowing the diameter of the vessels and increasing blood pressure.
In normal pregnancy, the uterus has lower RAS activity, producing less angiotensin II, which results in the blood vessels remaining dilated. This results in lower blood pressure and allows more oxygen and nutrients to pass from the mother's uterus to the placenta and fetus, which is beneficial for its development.
In preeclamptic women, however, the activity of the RAS is increased in the uterus, yet the mother's vessels remain dilated and the fetus' vessels constrict more than normal. Brosnihan and colleagues focused on uncovering the reason for this in the current study.