Background: Preeclampsia is characterized by a new onset of hypertension during pregnancy and is associated with autoantibodies against the angiotensin II type 1 receptor and oxidative stress. There is growing evidence for mitochondrial dysfunction in preeclampsia, however, the culprits for mitochondrial dysfunction are still being defined. We previously demonstrated that angiotensin II type 1 autoantibodies cause renal, placental, and endothelial mitochondrial dysfunction in pregnant rats.
View Article and Find Full Text PDFPreeclampsia (PE) is characterized by new-onset hypertension during pregnancy and is associated with immune activation and placental oxidative stress. Mitochondrial dysfunction is a major source of oxidative stress and may play a role in the pathology of PE. We (Vaka VR, et al.
View Article and Find Full Text PDFPlacental ischemia is believed to be the initial event in the development of preeclampsia. Mitochondrial dysfunction is a cause of reactive oxygen species (ROS) generation and oxidative stress, however, there are not many studies examining the role of mitochondrial ROS in the pathology of preeclampsia. The purpose of this study was to not only examine the effect of placental ischemia on mitochondrial-mediated oxidative stress in reduced uterine perfusion pressure (RUPP) rat model of preeclampsia but to also examine the role of mitochondrial ROS in contributing to hypertension in response to placental ischemia.
View Article and Find Full Text PDFBackground: Small observational studies have demonstrated that pre-eclampsia is associated with hypocalciuria.
Objectives: To compare urinary calcium excretion in pre-eclampsia, gestational hypertension, and chronic hypertension with that in normotensive pregnancies.
Search Strategy: Online databases were searched through February 2016 using medical subject headings "calcium homeostasis," "calcium excretion," "hypocalciuria," and "pre-eclampsia.