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. 2020 Apr 23:7:71.
doi: 10.3389/fcvm.2020.00071. eCollection 2020.

COVID and the Renin-Angiotensin System: Are Hypertension or Its Treatments Deleterious?

Florian Zores  1 , Mathieu E Rebeaud  2
Affiliations

COVID and the Renin-Angiotensin System: Are Hypertension or Its Treatments Deleterious?

Florian Zores et al. Front Cardiovasc Med. .
No abstract available

Keywords: 2019-nCoV; ACE2; COVID-19; SARS-CoV-2; angiotensin; renin.

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Figures

Figure 1
Figure 1
(A) ANGII binding to AT1R elevates blood pressure and promotes inflammation. ACE2 inactivates ANGII by converting it to ang-(–7) and negatively regulates the renin-angiotensin system, promoting vasodilatation and hypotension. (B) SARS-CoV-2 infection. Binding of SARS-CoV-2 with ACE2 leads to their internalization and to ACE2 shedding by ADAM17 (enzyme not shown). Lower availability of ACE2 results in a lower rate of ANGII degradation and excessive stimulation of AT1R, which facilitates ARDS and myocardial injury. Binding of ANGII to AT1R leads to membranous ACE2 internalization, decreasing ACE2 availability even more (not shown). Excessive ANGII is metabolized to ANGIV, which binds to AT4R and promotes thrombosis. Virus replication could also reduce cellular ACE2 expression (not shown). (C) SARS-CoV-2 infection and ACEi/ARB treatment. ACEi and ARB upregulate ACE2, and freer ACE2 remains after viral binding. ANGII is still degraded by ACE2 in its beneficial metabolite Ang-(–7), and AT1R and AT4R are less stimulated. ANGII binding on AT1R prevention with ARB and ANGII synthesis decrease with ACE lead to less AT1R stimulation and persistent interaction with ACE2, avoiding ACE2 internalization. ACE2, Angiotensin Converting Enzyme 2; ACEi, Angiotensin Converting Enzyme Inhibitor; ang-(–7), Angiotensin-(–7); ANGII, angiotensin II; ANGIV, angiotensin IV; ARB, Angiotensin Receptor Blocker; ARDS, Acute Respiratory Distress Syndrome; AT1R, Angiotensin II Type 1 Receptor; AT4R, Angiotensin II Type 4 Receptor; SARS-CoV-2, Severe Acute Respiratory Syndrome CoronaVirus 2.
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