论文部分内容阅读
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。
Preeclampsia is a unique disease during pregnancy, the current pathogenesis has not been fully elucidated. Pregnancy activates many components of the circulatory and uterine placental renin-angiotensin system (RAS). Studying the differences in RAS regulation between normal pregnancy and preeclampsia and uteroplacental units may help to elucidate the pathogenesis of preeclampsia. The changes of preeclampsia and uterine placenta RAS were reviewed. Different from normal pregnancy, many components of circulatory RAS in preeclampsia include AngⅠ, AngⅡ, Ang- (1-7) and plasma renin activity, serum angiotensin converting enzyme (ACE), serum AT1 itself Antibody (AT1-AA) increased. The concentration of total renin and active renin in the placenta was significantly increased, and the expression of AT1 receptor mRNA and protein was up-regulated. Uterine placental Ang Ang levels and renin, ACE mRNA was significantly increased.