Shah Dinesh M
Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, University of Wisconsin/Meriter, 202 S. Park Street, Madison, WI 53715, USA.
Curr Hypertens Rep. 2006 May;8(2):144-52. doi: 10.1007/s11906-006-0011-1.
Preeclampsia is a hypertensive disorder that is unique to pregnancy, with consistent involvement of the kidney. The renin-angiotensin system (RAS) has been implicated in the pathogenesis of preeclampsia. In the gravid state, in addition to the RAS in the kidney, there is a tissue-based RAS in the uteroplacental unit. Increased renin expression in human preeclampsia and in transgenic mouse models with a human preeclampsia-like syndrome shows that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. Vascular maladaptation in preeclampsia with increased vasomotor tone, endothelial dysfunction, and increased sensitivity to angiotensin II and norepinephrine in manifest preeclampsia may be explained on the basis of angiotensin II-mediated mechanisms through angiotensin receptor type I (AT1) activation. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT1 and bradykinin B2 receptor heterodimerization and the production of autoantibody against AT1. Various organ systems with predilection for involvement in preeclampsia are sites of tissue-based RAS. Angiotensin II-mediated mechanisms may explain the primary clinicopathologic features of preeclampsia. In this review, these various aspects are critically examined and an integrated concept on the role of RAS in preeclampsia is presented.
子痫前期是一种妊娠特有的高血压疾病，肾脏始终会受到影响。肾素 - 血管紧张素系统（RAS）与子痫前期的发病机制有关。在妊娠状态下，除了肾脏中的RAS外，子宫胎盘单位中还存在基于组织的RAS。人类子痫前期以及具有子痫前期样综合征的转基因小鼠模型中肾素表达增加表明，子宫胎盘RAS的激活，伴随着血管紧张素II进入体循环，可能介导子痫前期的发病机制。子痫前期的血管适应不良表现为血管运动张力增加、内皮功能障碍以及显性子痫前期中对血管紧张素II和去甲肾上腺素的敏感性增加，这可能基于血管紧张素II通过I型血管紧张素受体（AT1）激活介导的机制来解释。最近，子痫前期中描述了新的血管紧张素II相关生物分子机制。这些包括AT1和缓激肽B2受体异二聚化以及抗AT1自身抗体的产生。子痫前期中易受累的各种器官系统是基于组织的RAS的部位。血管紧张素II介导的机制可能解释子痫前期的主要临床病理特征。在本综述中，对这些各个方面进行了批判性审查，并提出了关于RAS在子痫前期中作用的综合概念。
