Abstract
Angiotensin-converting enzyme 2 (ACE2) is the receptor for COVID-19 (SARs-CoV-2). ACE2 protects the lung and heart from acute respiratory distress syndrome (ARDS) and acute myocarditis and arrhythmias, because it breaks down Angiotensin II, which has inflammatory effects in the lung and heart as well as in the kidney. When SARS-CoV-2 binds to ACE2, it suppresses it, so this protective action of ACE2 is lost. Death from COVID-19 is due to ARDS and also heart failure and acute cardiac injury. Drugs that prevent the inflammatory actions of Angiotensin II (i.e., Angiotensin receptor blockers, ARBs) prevent acute lung injury caused by SARS-CoV. Clinical trials are underway to test the risks and benefits of ARBs and angiotensin-converting enzyme inhibitors (ACEIs) in COVID-19 patients requiring hospitalization. Other potential treatments are also discussed.
Highlights
This article explains how the renin-angiotensin system (RAS) interacts with the severe acute respiratory syndrome coronavirus (SARS-CoV) and with the novel coronavirus, SARS-CoV-2, which causes infection and subsequent acute lung and probably heart injury [COVID-19 [1,2,3]]
As well as identifying potential therapeutic strategies for treating acute lung injury and myocarditis in COVID-19 [see [4,5,6]], this article provides a background to the management of patients with essential hypertension in accordance with recommendations made in the joint statement issued by the Heart Failure Society of America, the American College of Cardiology and the American Heart Association [7] that patients who are using drugs that block the RAS should continue to use them during this pandemic
The pro-inflammatory Angiotensin II (Ang II)-Ang II type 1 receptor (AT1R) is no longer blocked by the angiotensin-converting enzyme 2 (ACE2)-Ang–(1-7)Mas receptor (MasR) pathway and it is this imbalance that causes acute lung injury [13]
Summary
Angiotensin-converting enzyme 2 (ACE2) is the receptor for COVID-19 (SARs-CoV-2). ACE2 protects the lung and heart from acute respiratory distress syndrome (ARDS) and acute myocarditis and arrhythmias, because it breaks down Angiotensin II, which has inflammatory effects in the lung and heart as well as in the kidney. When SARS-CoV-2 binds to ACE2, it suppresses it, so this protective action of ACE2 is lost. Death from COVID-19 is due to ARDS and heart failure and acute cardiac injury. Drugs that prevent the inflammatory actions of Angiotensin II (i.e., Angiotensin receptor blockers, ARBs) prevent acute lung injury caused by SARS-CoV. Clinical trials are underway to test the risks and benefits of ARBs and angiotensin-converting enzyme inhibitors (ACEIs) in COVID-19 patients requiring hospitalization.
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