Preeclampsia (PE) is a hypertensive syndrome (blood pressure above 140/90 mmHg, after 20 weeks of conception) that affects 4 to 7% of all pregnancies. The genitors and fetuses with this abnormality have greater propensity to develop chronic diseases in the future. The incubation of endothelial cells with plasma of preeclamptic women is seen as an in vitro model to investigate this disorder, based on the link between placental ischemia/hypoxia that releases factors in the circulation that can act on the maternal endothelium, compromising their function. During PE there is a reduction in nitric oxide (NO) levels, a vasodilating substance derived from the endothelium, whose level is decreased in endothelial dysfunction, contributing to oxidative stress. Recent researches have demonstrated the participation of hydrogen sulfide (H2S), a gaseous molecule, in cardiovascular functions. It shares several structures and functions with the NO, responding to various stimulus, quoting, regulating vascular contractility and its structural integrity, promoting a profound impact on angiogenesis. In a significant way, studies have expressed that the decrease in plasma levels of H2S or its production enzymes occurs in the PE, while demonstrating how it promoted the phosphorylation of ENOS in endothelial cells with consequent increase in the synthesis of NO, evidencing the crosstalk between these two gases. Thus, we look forward to investigating how H2S acts in the bioavailability of NO, besides analyzing whether it has any correlation with the manifestation of oxidative stress in a pre-eclampsia in vitro model.
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