子宫胎盘单位的肾素-血管紧张素系统与子痫前期

Renin Angiotensin System in the Uteroplacental Unit and Pre-eclampsia

子痫前期是妊娠期特有疾病,目前发病机制尚未完全阐明。妊娠激活了循环和子宫胎盘单位肾素-血管紧张素系统(RAS)的许多组分。研究正常妊娠和子痫前期循环及子宫胎盘单位中RAS调节的差异有助于探讨子痫前期的发病机制。就子痫前期循环和子宫胎盘RAS的变化进行综述。与正常妊娠者不同,子痫前期患者循环RAS的许多组分包括AngⅠ、AngⅡ、Ang-(1-7)及血浆肾素活性下调,血清血管紧张素转换酶(ACE)增加,血清中AT1自身抗体(AT1-AA)增高。胎盘中的总肾素和活性肾素浓度显著升高,AT1受体mRNA、蛋白的表达上调。子宫胎盘床中AngⅡ水平及肾素、ACE mRNA显著升高。

Pre-eclampsia is a pregnancy-specific disease. The pathogenic mechanisms of pre-eclampsia remain largely undefined. Pregnancy activates many of the different components of circulating and local renin angiotensin system （RAS）. Research on the different regulation of RAS between normal pregnant and pre- eclampsia may provide insight into the pathogenesis of pre-eclampsia. In this article, we reviewed literatures on the changes of RAS in circulation and uteroplacental unit in Pre-eclampsia. Unlike in normal pregnancies, many components in circulating RAS, including Ang Ⅰ , Ang Ⅱ , Ang-（1-7）, and plasma renin activity were downregulated in women with pre-eclampsia, sera ACE and AT1 antibodies（AT1-AA） also increased. In pre- eclamptie placenta, total renin and active renin concentration significantly increased, and AT1 receptor mRNA, protein were also upregulated.Ang Ⅱ peptide levels, renin activity and ACE mRNA in utenine placental bed were significantly increased.