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首页> 外文期刊>American Journal of Physiology >Role of the renin-angiotensin system in the pathogenesis of preeclampsia.
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Role of the renin-angiotensin system in the pathogenesis of preeclampsia.

机译：肾素-血管紧张素系统在先兆子痫发病机理中的作用。

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Preeclampsia is a hypertensive disorder 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 observed both in human preeclampsia and in a transgenic mouse model with a human preeclampsia-like syndrome supports the concept that activation of the uteroplacental RAS, with angiotensin II entering the systemic circulation, may mediate the pathogenesis of preeclampsia. A novel disease paradigm of the two-kidney one-clip (2K-1C) Goldblatt model is presented for preeclampsia, wherein the gravid uterus is the clipped "kidney" and the two maternal kidneys represent the unclipped kidney. Validation of the 2K-1C Goldblatt model analogy requires evidence of elevated angiotensin II in the peripheral circulation before vascular maladaptation in preeclampsia. Convincing evidenceof the elevation of angiotensin II in preeclampsia does not exist despite the fact that much of vascular pathogenesis appears to be due to angiotensin type I (AT(1)) receptor activation. Vascular maladaptation 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. Recently, novel angiotensin II-related biomolecular mechanisms have been described in preeclampsia. These include AT(1) and bradykinin B(2) receptor heterodimerization and the production of an autoantibody against AT(1). Various organ systems with a predilection for involvement in preeclampsia are each a site of a tissue-based RAS. How angiotensin II-mediated mechanisms may explain the primary clinical-pathological features of preeclampsia is described. Future investigations are proposed to more precisely define the role of activation of the uteroplacental RAS in the mechanisms underlying preeclampsia.
机译：子痫前期是妊娠期独有的高血压疾病，肾脏持续受累。肾素-血管紧张素系统（RAS）与先兆子痫的发病机理有关。在妊娠状态下，除了肾脏中的RAS外，子宫胎盘单元中还存在基于组织的RAS。在人先兆子痫和具有人先兆子痫样综合征的转基因小鼠模型中观察到的肾素表达增加支持以下观念：子宫胎盘RAS的激活，血管紧张素II进入体循环，可能介导先兆子痫的发病机理。提出了一种适用于先兆子痫的两肾一夹（2K-1C）Goldblatt模型的新型疾病范例，其中妊娠子宫是被修剪的“肾脏”，两个母体肾脏代表了未被修剪的肾脏。 2K-1C Goldblatt模型类似物的验证需要先兆子痫前的血管适应不良之前外周循环血管紧张素II升高的证据。尽管事实上许多血管发病机制似乎是由于I型血管紧张素（AT（1））受体激活引起的，但子痫前期中血管紧张素II升高的令人信服的证据并不存在。子痫前期表现为子痫前期伴血管舒张张力增高，内皮功能障碍和对血管紧张素II和去甲肾上腺素敏感性增加的血管适应不良可能是由血管紧张素II介导的机制引起的。最近，先兆子痫中已经描述了新的与血管紧张素II相关的生物分子机制。这些包括AT（1）和缓激肽B（2）受体异二聚化以及针对AT（1）的自身抗体的产生。倾向于参与先兆子痫的各种器官系统均是基于组织的RAS的部位。描述了血管紧张素II介导的机制如何解释先兆子痫的主要临床病理特征。提出了进一步的研究，以更精确地定义子宫胎盘RAS激活在先兆子痫的潜在机制中的作用。

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