School of Biomedical Sciences and Pharmacy and Mothers and Babies Research Centre, Hunter Medical Research Institute, University of Newcastle, Newcastle, New South Wales, Australia.
Am J Physiol Regul Integr Comp Physiol. 2014 Jan 15;306(2):R91-101. doi: 10.1152/ajpregu.00034.2013. Epub 2013 Oct 2.
This review describes the changes that occur in circulating renin-angiotensin-aldosterone system (RAAS) components in human pregnancy. These changes depend on endocrine secretions from the ovary and possibly the placenta and decidua. Not only do these hormonal secretions directly contribute to the increase in RAAS levels, they also cause physiological changes within the cardiovascular system and the kidney, which, in turn, induce reflex release of renal renin. High levels of ANG II play a critical role in maintaining circulating blood volume, blood pressure, and uteroplacental blood flow through interactions with the ANG II type I receptor and through increased production of downstream peptides acting on a changing ANG receptor phenotype. The increase in ANG II early in gestation is driven by estrogen-induced increments in angiotensinogen (AGT) levels, so there cannot be negative feedback leading to reduced ANG II production. AGT can exist in various forms in terms of redox state or complexed with other proteins as polymers; these affect the ability of renin to cleave ANG I from AGT. Thus, during pregnancy the rate of ANG I production varies not only because levels of renin change in response to homeostatic demand but also because AGT changes not only in concentration but in form. Activation of the circulating and intrarenal RAASs is essential for normal pregnancy outcome subserving the increased demand for salt and, hence, water during pregnancy. Thus, the complex integration of the secretions and actions of the circulating maternal renin-angiotensin system in pregnancy plays a key role in pregnancy outcome.
这篇综述描述了人类妊娠期间循环肾素-血管紧张素-醛固酮系统（RAAS）成分的变化。这些变化取决于卵巢和可能的胎盘和蜕膜的内分泌分泌。这些激素分泌不仅直接导致 RAAS 水平的增加，还导致心血管系统和肾脏的生理变化，进而引起肾素的反射释放。高水平的 ANG II 通过与 ANG II 型 1 受体相互作用以及通过增加作用于变化的 ANG 受体表型的下游肽的产生，在维持循环血容量、血压和胎盘血流方面发挥关键作用。妊娠早期 ANG II 的增加是由雌激素诱导的血管紧张素原（AGT）水平增加驱动的，因此不会产生导致 ANG II 产生减少的负反馈。AGT 可以在氧化还原状态或与其他蛋白质形成聚合物的形式方面存在多种形式；这些会影响肾素从 AGT 中切割 ANG I 的能力。因此，在怀孕期间，ANG I 产生的速度不仅因为肾素水平根据体内平衡需求而变化，而且因为 AGT 不仅在浓度而且在形式上发生变化。循环和肾内 RAAS 的激活对于正常妊娠结局至关重要，因为妊娠期间对盐的需求增加，因此对水的需求也增加。因此，母体肾素-血管紧张素系统在妊娠期间的分泌和作用的复杂整合在妊娠结局中起着关键作用。
