Maternal and Fetal Complications Due to Decreased Nitric Oxide Synthesis during Gestation

Abstract

Nitric oxide (NO) is synthesized from L-arginine by the constitutive NO synthase in vascular endothelial cells and plays an important role in the regulation of blood pressure and coronary vasomotion. Normal pregnancy is associated with major adaptations in maternal cardiovascular function, which help the woman to accommodate the growing fetus. The vascular endothelium is stimulated during pregnancy to release increased amounts of NO, and the abnormality in the L-arginine NO pathway may play a role in the etiology of preeclampsia. The objective of this study is to discuss the importance of nitric oxide during gestation and the maternal and fetal complications associated with decreased NO synthesis during this period. Maternal arterial hypertension due to inhibition of nitric oxide synthesis during pregnancy impairs fetal development, mainly the reduction of the wall/lumen ratio of the cardiac and renal microvasculature as well as the reduction in the number of nephrons. These changes may contribute to the development of hypertension. Despite these findings, more studies are needed to understand the programming of fetal development, and the intrauterine environmental factors. influence this process.

The Pivotal Role of the Placenta in Normal and Pathological Pregnancies: A Focus on Preeclampsia, Fetal Growth Restriction, and Maternal Chronic Venous Disease

“…The diminished NO production is also potentially related to the reduced bioavailability of its precursor, L-arginine, both being observed in women with PE [159]. These alterations may promote changes in the renal and cardiac microvasculature as well as a reduction in the number of fetal nephrons in vivo, which can possibly also occur in humans [160]. Notwithstanding, a clear implication of oxidative stress is seen in the etiopathogenesis of PE: the use of antioxidants such as vitamin C, E, or n-acetylcysteine has failed to show any clinical benefit [161].…”

The Pathophysiology of Preeclampsia and Eclampsia

“…As a result, maternal plasma volume expansion begins in the first trimester, resulting in a subsequent decrease in plasma osmolality, and this expansion continues until around 32 weeks [159]. The maintenance of maternal blood volume is essential for fetal development [158], and overall blood and plasma volumes are reduced in those with preeclampsia despite elevations in blood pressure [160,161]. In these hypovolemic women, body fluid is distributed more to the interstitial space rather than the intravascular space, which is indicative of capillary leak [162][163][164] and paralleled in the deoxycorticosterone acid salt rat model of preeclampsia [165].…”

Exploring the Role of Mediterranean and Westernized Diets and Their Main Nutrients in the Modulation of Oxidative Stress in the Placenta: A Narrative Review

“…These markers aid in the early diagnosis of disease and the avoidance of serious problems, since they are typically linked to the angiogenic growth of the placenta [63]. These modifications may encourage changes in the renal and cardiac microvasculature, as well as a decrease in the number of embryonic nephrons in vivo, which may also take place in humans [64]. Notably, the utilization of antioxidants such as vitamin C, vitamin E, or n-acetylcysteine has not demonstrated any discernible therapeutic benefits in the management of this condition [65].…”