The discovery of angiotensin converting enzyme-2 (ACE-2) as the receptor for SARS- CoV-2 (Severe Acute Respiratory Syndrome Coronavirus-2) has implicated the renin-angiotensin-aldosterone system in acute respiratory distress syndrome (ARDS) and respiratory failure in patients with coronavirus disease-19 (COVID-19). The angiotensin converting enzyme-1-angiotensin II-angiotensin AT1 receptor pathway contributes to the pathophysiology of ARDS, whereas activation of the ACE-2-angiotensin(1-7)-angiotensin AT2 receptor and the ACE-2-angiotensin(1-7)-Mas receptor pathways have been shown to be protective. Here we propose and discuss therapeutic considerations how to increase soluble ACE-2 in plasma in order for ACE-2 to capture and thereby inactivate SARS-CoV-2. This could be achieved by administering recombinant soluble ACE-2. We also discuss why and how ACEIs and ARBs provide cardiovascular, renal and also pulmonary protection in SARS-CoV-2- associated ARDS. Discontinuing these medications in COVID-19 patients may therefore potentially be harmful.
KEYWORDS: ACE, ACE inhibitor, ACE inhibitors, ACE-2, ACEIs, ARBs, ARDS, Acute respiratory distress syndrome, COVID-19, RAAS, SARS, SARS-CoV-2, angiotensin, angiotensin receptor antagonists, angiotensin receptor blocker, angiotensin-converting enzyme-1, angiotensin-converting enzyme-2, arterial hypertension, cardiovascular, coronavirus, human biology, infection, medicine, renin-angiotensin-aldosterone system, therapy, treatment, virus