Preeclampsia is a common disease of pregnancy characterized by the presence of hypertension and commitment of many organs, including the brain, secondary to generalized endothelial dysfunction. Its etiology is not known precisely, but it involved several factors, highlighting the renin angiotensin system (RAS), which would have an important role in the origin of multisystem involvement. This paper reviews the evidence supporting the involvement of RAS in triggering the disease, in addition to the components of this system that would be involved and how it eventually produces brain engagement. 1. Introduction Preeclampsia is a major complication of pregnancy and corresponds to a major cause of both maternal and fetal morbidity and mortality [1–3]. It is a condition that produces a compromise of many organs, including the brain causing seizures, a condition known as eclampsia [4, 5]. The pathophysiology is not well understood, but it involves different factors, such as genetic, immunological, and inflammatory [6, 7]. In recent years there is a series of studies linking the renin angiotensin system (RAS) with preeclampsia [8–10], in the sense that the alteration of this system would be involved in the pathogenesis of this disease, as this could trigger the different characteristics in this pathology, including brain involvement. 2. RAS in Normal Pregnancy RAS is a system that functions as an important regulator of blood pressure, electrolyte balance, and fluid homeostasis . This system comprises the inactive peptide angiotensinogen, which is converted to angiotensin I and then the active peptide angiotensin II (Ang II) through the action of renin and angiotensin-converting enzyme (ACE) . Ang II exerts its action primarily through the AT1 receptor, located widely in different tissues, including the syncytiotrophoblast . During pregnancy usually occurs overexpression of many components of the RAS, both in the blood and tissues. There is an increase in plasma renin mainly by extrarenal production . There is also a higher-level production of angiotensinogen liver secondary to increased circulating estrogens. ACE is the only component that has been shown to decrease during normal pregnancy, but equally there is a higher plasma concentration of Ang II [8, 13]. There is an upregulation of RAS components during normal pregnancy, but there is also a decrease in sensitivity to Ang II, whereby these women are resistant to the pressor effect of this molecule, requiring twice Ang II by intravenous infusion compared with nonpregnant women to achieve a
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