Preeclampsia, the most frequent, serious, hypertensive complication of
pregnancy, occurs in about 5 to 8% of all live-birth pregnancies in the United States.
Despite being one of the leading causes of maternal death and a major contributor of
maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of
preeclampsia are unknown. Development of an animal model that recapitulates this
complex pregnancy-related disorder may help to expand our understanding and may
hold great potential for the design and implementation of effective treatment. There
have been numerous attempts to generate animal models of preeclampsia. An ideal
animal model of this disease would exhibit all the symptoms seen in preeclamptic
women: hypertension, proteinuria, endothelial dysfunction including glomerular
endotheliosis, and imbalance of angiogenic factors. Finding a model that satisfies these
criteria has been very challenging. In this chapter we will discuss new disease models
that have been created to tackle this complex and devastating disorders.
Keywords: Preeclampsia, animal models, rodents, angiogenesis, hypertension,
proteinuria, endotheliosis, endothelial dysfunction, trophoblast invasion, vascular
endothelial growth factor (VEGF), soluble receptors for VEGF 1, nitric oxide,
statins, angiotensin, complement component C1q, uterine perfusion.
