Further experiments revealed that stimulation of type 1 receptors (AT1) for Ang II, NADPH (nicotinamide adenine dinucleotide phosphate) oxidase activity and SGLT1- and SGLT2-dependent mechanisms act in concert to induce endothelial dysfunction and a pro-coagulation state by means of a downregulated function of endothelial nitric oxide (NO) synthase, impaired NO synthesis and the increased synthesis of adhesion molecules, tissue factor, monocyte chemoattractant protein-1 (MCP-1) and beta-galactosidase activity (the latter serving as a marker of cellular senescence) [23]. Here, CCL2 is linked to endothelial dysfunction.