PP074. Characteristic changes in endothelial function in uterine artery by administration of no synthase inhibitor during period of placental formation

Abstract

Preeclampsia is characterized as an increased peripheral vascular resistance. It is found that the administration of the NOS inhibitor l-NAME at early pregnancy developed hypertension in rats similar to preeclampsia. Furthermore, we found action of endothelial NO was reduced due to possibly reactive oxygen species (ROS) in preeclamptic women. We investigated whether this treatment modulates NO and ROS production in uterine artery endothelial cells at late pregnancy in rats. l-NAME was continuously administered during the 8-14th day of gestation in Wistar rats. Blood pressure was meassured by use of tail-cuff method. The uterine artery was obtained at the 20th day of gestation. Acetylcholine (ACh)-induced endothelial NO production was estimated from DAF-2 fluorescence. Furthermore, ACh-induced endothelial cell ROS production was estimated from CM-H2 DCFDA by fluorescence imaging system. Blood pressure was higher and birth body weight was smaller in l-NAME-treated rats than in saline-treated rats. Acetylcholine (ACh)-induced endothelial NO production was higher, while ACh-induced endothelial cell ROS production was similar, in l-NAME-treated rats when compared with those in control rats. It is suggested that the increased endothelial NO production in the uterine artery seen by a short term administration of l-NAME to rats during early pregnancy may function to protect the development of hypertension.