In addition, both sotagliflozin and empagliflozin prevented the Ang II-induced down-regulation of eNOS and formation of NO in response to bradykinin, and the up-regulation of VCAM-1, MCP-1 and tissue factor indicating a determinant role of SGLT1 and 2 in the induction of endothelial dysfunction (Fig. 5c–f and i). This evidence concerns the gene SLC5A1 and endothelial dysfunction.