Characteristic changes of endothelial function in preeclampsia model rat by administration of nitric oxide synthase inhibitor

先兆子痫的特征是外周血管阻力增加。研究发现，在妊娠早期给予一氧化氮合酶抑制剂L-NAME，大鼠会出现类似于先兆子痫的高血压。此外，我们还发现，在子痫前期妇女中，内皮一氧化氮(NO)的作用可能是由于活性氧(ROS)的作用而减少的。我们研究了该药是否调节妊娠晚期大鼠子宫动脉内皮细胞NO和ROS的产生。与对照组相比，L治疗组大鼠血压更高，出生体重更小。L治疗组大鼠滋养层侵袭减少。与对照组相比，L组大鼠ACh诱导的内皮细胞NO生成增加，内皮细胞ROS生成和钙增加相似。提示L治疗组大鼠子宫动脉内皮细胞NO生成量增加，可能对高血压的发生有保护作用。

Preeclampsia is characterized as an increased peripheral vascular resistance. It is found that administration of the NOS inhibitor L-NAME at early pregnancy developed hypertension in rat similar to preeclampsia. Furthermore, we found action of endothelial nitric oxide (NO) was reduced due to possibly reactive oxygen species (ROS) in preeclamptic women. We investigated whether this administration modulates NO and ROS production in uterine artery endothelial cells at late pregnancy in rat.Blood pressure was higher and birth body weight was smaller in L-NAME-treated rats than in control rats. Trophoblast invasion was reduced in L-NAME-treated rats. ACh-induced endothelial NO production was higher, while endothelial cell ROS production and Ca increase was similar, in L-NAME-treated rats when compared with those in control rats. It is suggested that the increased endothelial NO production in uterine artery seen in L-NAME-treated rats may function to protect the development of hypertension.