AGT and endothelial dysfunction: RAAS mediates two principal biological pathways: (1) converting Ang I into Ang II (acting at the Ang II type 1 receptor contributing to blood pressure increases through renal water, vasoconstriction, and sodium reabsorption increase and endothelial dysfunction via the stimulation of proinflammatory cytokines leading to inflammation promotion); (2) the utilization of ACE2 to generate Ang 1-7 (acting at the Mas receptor, contributing to inflammation and blood pressure reduction) [32].