Dinesh M Shah1. 1. University of Wisconsin School of Medicine and Public Health, Meriter Hospital, Madison, Wisconsin 53715, USA. dmshah@wisc.edu
Abstract
PURPOSE OF REVIEW: Preeclampsia is a disorder of gestation characterized by hypertension and proteinuria and can be complicated by eclamptic seizures. This review describes recent advances in the role of the renin-angiotensin system and angiogenic and anti-angiogenic factors of placental origin in its pathogenesis. RECENT FINDINGS: Deficient uteroplacental perfusion has been recognized to be a feature in all preeclampsia syndromes. Increased renin expression observed in humans and animal models supports the concept that activation of the decidual renin-angiotensin system may mediate the pathogenesis of preeclampsia. Novel angiotensin II-related biomolecular mechanisms, angiotensin II type 1-B2 receptor heterodimerization and autoantibody against angiotensin II type 1 have recently been described in preeclampsia. New evidence suggests that vascular endothelial growth factor and its receptors, antagonists, and reduced placental growth factor may play a role in the development of proteinuria and other renal injury-mediated manifestations in preeclampsia. SUMMARY: Vascular maladaptation, with increased vasomotor tone, endothelial dysfunction, increased sensitivity to angiotensin II and norepinephrine, and multiorgan dysfunction seen in preeclampsia, may be explained by angiotensin II-mediated mechanisms. Future investigations need to define the mechanism of activation of the decidual renin-angiotensin system and the release of placental factors in the pathogenesis of preeclampsia.
PURPOSE OF REVIEW: Preeclampsia is a disorder of gestation characterized by hypertension and proteinuria and can be complicated by eclamptic seizures. This review describes recent advances in the role of the renin-angiotensin system and angiogenic and anti-angiogenic factors of placental origin in its pathogenesis. RECENT FINDINGS: Deficient uteroplacental perfusion has been recognized to be a feature in all preeclampsia syndromes. Increased renin expression observed in humans and animal models supports the concept that activation of the decidual renin-angiotensin system may mediate the pathogenesis of preeclampsia. Novel angiotensin II-related biomolecular mechanisms, angiotensin II type 1-B2 receptor heterodimerization and autoantibody against angiotensin II type 1 have recently been described in preeclampsia. New evidence suggests that vascular endothelial growth factor and its receptors, antagonists, and reduced placental growth factor may play a role in the development of proteinuria and other renal injury-mediated manifestations in preeclampsia. SUMMARY: Vascular maladaptation, with increased vasomotor tone, endothelial dysfunction, increased sensitivity to angiotensin II and norepinephrine, and multiorgan dysfunction seen in preeclampsia, may be explained by angiotensin II-mediated mechanisms. Future investigations need to define the mechanism of activation of the decidual renin-angiotensin system and the release of placental factors in the pathogenesis of preeclampsia.