Role of nitric oxide in the pathophysiology of pregnancy-induced hypertension

Abstract

Background: Pregnancy-induced hypertension (PIH) is a major cause of morbidity and mortality during pregnancy. Previous research suggests that endothelial dysfunction is important in the pathogenesis of PIH and may lead to alterations in nitric oxide (NO) synthesis. As endothelial cell damage is considered pivotal in the pathogenesis of pre-eclampsia, this study was initiated to determine whether NO production is decreased in patients with PIH. Objective: The objectives of this study were to determine the role of NO levels on the increased vascular resistance in the pathophysiology of PIH. Materials and methods: A case–control study was conducted. A total of 60 women in the second trimester of pregnancy with PIH and 60 healthy, normotensive women in second trimester matched with respect to maternal age, gestational age, and body mass index were selected. The resting blood pressure of the subjects was recorded on 2 consecutive days, and the average of the two values was recorded. Fasting blood samples of the subjects was obtained for the estimation of NO levels. Results: The mean serum NO levels of both the groups were compared. A decrease was observed in the mean serum NO levels (μM) in subjects with PIH (18.5 ± 5.8) compared with the controls (36.9 ± 3.9). The difference was statistically significant at P < 0.05. Conclusion: The present study shows a significantly less level of serum NO in women in their second trimester of pregnancy with PIH compared to the controls. This finding may be one of the major clues in unravelling the role of endothelial dysfunction in the pathophysiology of PIH and hence aid in its management.