C Ma1, Y Zhuang, Y Xu. 1. Obstetrics and Gynecology Hospital, Shanghai Medical University, Shanghai 200011.
Abstract
OBJECTIVE: To study the effect of the inhibition of nitric oxide(NO) synthesis on plasma endothelin (ET), prostaglandlin I2(PGI2), thromboxane (TXA2) and angiotensin (ANGII) in pregnant rats, and to investigate the role of these factors in the pathogenesis of pregnancy-induced hypertension(PIH). METHODS: Pregnant rats were divided into two groups randomly. Saline solution or L-nitro arginine methyl ester (L-NAME) 125 mg/day was given subcutaneously from day 14 of gestation till delivery. Systolic blood pressure, urine protein, platelet count, and weight of pups and placentae were determined. Plasma NO, ET, PGI2, TXA2 and ANGII were measured by RIA. RESULTS: Pregnant rats which were given L-NAME produced physical signs similar to those of PIH, such as increase in systolic blood pressure (140.6 +/- 3.8) mmHg and urine protein (801.38 +/- 57.12) mg/L, and decrease in platelet count (533 +/- 42) x 10(9)/L and weight of pups and placentae. Compared with controls, plasma NO, PGI2 and ANG II were decreased significantly while plasma ET and TXA2 were increased significantly in rats given L-NAME. CONCLUSION: Inhibition of NO synthesis can cause imbalance of several vaso-regulatory factors, which may be responsible for the pathogenesis of PIH.
OBJECTIVE: To study the effect of the inhibition of nitric oxide(NO) synthesis on plasma endothelin (ET), prostaglandlin I2(PGI2), thromboxane (TXA2) and angiotensin (ANGII) in pregnant rats, and to investigate the role of these factors in the pathogenesis of pregnancy-induced hypertension(PIH). METHODS: Pregnant rats were divided into two groups randomly. Saline solution or L-nitro arginine methyl ester (L-NAME) 125 mg/day was given subcutaneously from day 14 of gestation till delivery. Systolic blood pressure, urine protein, platelet count, and weight of pups and placentae were determined. Plasma NO, ET, PGI2, TXA2 and ANGII were measured by RIA. RESULTS: Pregnant rats which were given L-NAME produced physical signs similar to those of PIH, such as increase in systolic blood pressure (140.6 +/- 3.8) mmHg and urine protein (801.38 +/- 57.12) mg/L, and decrease in platelet count (533 +/- 42) x 10(9)/L and weight of pups and placentae. Compared with controls, plasma NO, PGI2 and ANG II were decreased significantly while plasma ET and TXA2 were increased significantly in rats given L-NAME. CONCLUSION: Inhibition of NO synthesis can cause imbalance of several vaso-regulatory factors, which may be responsible for the pathogenesis of PIH.