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Fig. 1 | Critical Care

Fig. 1

From: COVID-19 and the RAAS—a potential role for angiotensin II?

Fig. 1

Effect of angiotensin II on the RAAS and SARS-CoV-2 binding. Angiotensin I is hydrolyzed by ACE1 to form angiotensin II, which binds to AT1 receptors. This causes release of aldosterone from the adrenal gland, vasopressin secretion from the hypothalamus, and vasoconstriction. Vasopressin and aldosterone both lead to increased sodium and free water reabsorption in the kidney, leading to increased mean arterial pressure (MAP). Angiotensin II is then metabolized into Ang-(1–7) by ACE2. SARS-CoV-2 binds to ACE2 to gain entry into the host cell. Exogenous angiotensin II can also bind to ACE2, which can lead to competitive inhibition of the ACE2 receptor. In addition, binding of angiotensin II to AT1 receptors leads to internalization, downregulation, and degradation of ACE2. These actions may potentially prevent SARS-CoV2 from entering the cell. Figure created with Motifolio Toolkit. Ang-2, angiotensin II; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; ACE1, angiotensin-converting-enzyme 1; ACE2, angiotensin-converting-enzyme 2; H2O, water; Na+, sodium

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