Shah Dinesh M
University of Wisconsin School of Medicine and Public Health, Meriter Hospital, Madison, Wisconsin 53715, USA.
Curr Opin Nephrol Hypertens. 2007 May;16(3):213-20. doi: 10.1097/MNH.0b013e3280d942e9.
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.
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.
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.
子痫前期是一种妊娠期疾病，其特征为高血压和蛋白尿，可并发子痫发作。本综述描述了肾素 - 血管紧张素系统以及胎盘来源的血管生成和抗血管生成因子在其发病机制中的作用的最新进展。
子宫胎盘灌注不足已被公认为所有子痫前期综合征的一个特征。在人类和动物模型中观察到的肾素表达增加支持这样一种概念，即蜕膜肾素 - 血管紧张素系统的激活可能介导子痫前期的发病机制。最近在子痫前期中描述了新型血管紧张素 II 相关生物分子机制、血管紧张素 II 1 - B2 型受体异二聚化以及抗血管紧张素 II 1 型自身抗体。新证据表明，血管内皮生长因子及其受体、拮抗剂以及胎盘生长因子减少可能在子痫前期蛋白尿和其他肾损伤介导的表现的发展中起作用。
子痫前期中出现的血管适应不良，表现为血管运动张力增加、内皮功能障碍、对血管紧张素 II 和去甲肾上腺素的敏感性增加以及多器官功能障碍，可能由血管紧张素 II 介导的机制来解释。未来的研究需要确定蜕膜肾素 - 血管紧张素系统的激活机制以及胎盘因子在子痫前期发病机制中的释放情况。
