Abstract
To assess the influence of oxidative stress on the gene expression of nitric oxide synthases (NOS 3 and NOS 2) and, hence, the cardiovascular responses in preeclampsia. This was a case control study in which patients with preeclampsia (PE group) and normal pregnancy controls (NP group) were included according to the guidelines of the American College of Obstetricians and Gynecologists (ACOG). The serum levels of malondialdehyde (MDA), total antioxidant capacity, and nitric oxide (NO) were estimated, and the heart rate and mean arterial pressure were recorded. The gene profiling of NOS3 and NOS2 was performed through real-time polymerase chain reaction (RT-PCR). The statistical analysis was performed using the Student t-test, and values of p < 0.05 were considered statistically significant. The serum levels of malondialdehyde were increased (p < 0.0001), and the total antioxidant capacity was reduced in the PE group (p = 0.034), indicating oxidative stress. In the PE group, the mean arterial pressure was significantly higher (p < 0.0001), but the serum levels of NO did not show a statistically significant reduction (p = 0.20). The gene expression profiling of NOS3 and NOS2 revealed a down regulation in the PE group by 8.49 and 51.05 times respectively. Oxidative stress may lead to endothelial dysfunction, which could result in increased mean arterial pressure. Nitric oxide may play a role in this mechanism, but interactions with other vasoactive /biological substances cannot be overlooked, as the gene expression of NOS3 and NOS2 has been reduced.
Highlights
Normal pregnancy is marked by systemic inflammation, oxidative stress, and changes in angiogenic factors and vascular reactivity
The gene expression profiling of NOS3 and NOS2 revealed a down regulation in the PE group by 8.49 and 51.05 times respectively
Oxidative stress may lead to endothelial dysfunction, which could result in increased mean arterial pressure
Summary
Normal pregnancy is marked by systemic inflammation, oxidative stress, and changes in angiogenic factors and vascular reactivity. This phenomenon is very much increased in pre-eclampsia (PE), with an impairment of compensatory mechanisms, eventually leading to vascular dysfunction.[1] The pathophysiology of PE is not completely understood. Nitric oxide (NO) may be responsible for gestational vasodilation due to its vasodilator action.[2] The production of NO from L-arginine is catalyzed by nitric oxide synthases (NOSs), which include neuronal NOS, endothelial NOS (eNOS/NOS3) and inducible NOS (iNOS/NOS2).[3]. Reduced uterine perfusion pressure (RUPP) and placental ischemia may lead to endothelial and cardiovascular dysfunction through increased production of cytokines, which may trigger endothelial dysfunction by decreasing the bioavailability of NO and increasing that of reactive oxygen species (ROSs).[4]
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