ACE2 (angiotensin-converting enzyme) is a critical component of the counter-regulatory pathway of the RAAS, that regulators blood pressure, inflammation, and fibrosis and is crucial to the pathophysiology of hypertension, cardiovascular disease, and chronic kidney disease. ACE2 converts Ang II into Ang-(1–7), which lower blood pressure and reduce inflammation and fibrosis. Ang-(1–7)’s primary actions are to promote vasodilation and sodium and water excretion, reduce sympathetic nervous system tone, and increase nitric oxide production.
ACE2 is the SARS-CoV-2 binding site. The unique interaction of SARS-CoV-2 with the host cell is the putative link between COVID-19 and hypertension, cardiovascular disease, and kidney disease. As with SARS-CoV, the SARS-CoV-2 spike protein binds to membrane-bound ACE2 on the surface of respiratory epithelial cells to gain cell entry, although SARS-CoV-2 appears to do so with significantly greater affinity. Endocytosis of the SARS-CoV-2–ACE2 complex, as well as viral-induced ACE2 cell surface shedding and ACE2 downregulation, all may contribute to decreased ACE2 expression and activity in infected cells. This overall loss of ACE2 functionality could be critically important to COVID-19 pathophysiology. 
 A. M. South, T. M. Brady, and J. T. Flynn, “ACE2 (Angiotensin-Converting Enzyme 2), COVID-19, and ACE Inhibitor and Ang II (Angiotensin II) Receptor Blocker Use During the Pandemic: The Pediatric Perspective,” Hypertens. (Dallas, Tex. 1979), vol. 76, no. 1, pp. 16–22, 2020, doi: 10.1161/HYPERTENSIONAHA.120.15291.
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