Some circulatory pathophysiological traits (hypertension, endothelial dysfunction) in patients with severe COVID-19 were rapidly linked to RAAS changes, as the balance between the two arms (ACE-ANGII-Angiotensin II Type 1 receptor (AT1R) versus ACE2-Ang1–7-Mas receptor) of the system could change significantly if ACE2 abundance or activity is lowered by SARS-CoV-2 infection and renin secretion increased. Here, AGTR1 is linked to endothelial dysfunction.