Some of the mediators of endothelial dysfunction include reduced bioavailable NO, increased production of vasoconstrictors, such as endothelin-1 and angiotensin II, and dysregulated inflammation or thrombosis (DeFronzo et al., 2015; Palmer A.K. et al., 2015; Yan-Do and MacDonald, 2017; Alves et al., 2019; Kruger-Genge et al., 2019; Rashvand et al., 2019; Giraldo-Grueso and Echeverri, 2020). This evidence concerns the gene AGT and endothelial dysfunction.