Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) is the virus responsible for the coronavirus disease 2019 (COVID-19) pandemic. The angiotensin-converting enzyme 2 (ACE2) has been proven to be used by SARS-CoV-2 for host cell entry. Considering that angiotensin receptor blockers and ACE inhibitors (ACEIs) upregulate the expression of ACE2 in animal studies, there may be a concern about whether these drugs may increase COVID-19 susceptibility and severity. Recently, there has been a debate among clinicians about whether to continue or to stop ACEIs and angiotensin receptor blockers in the context of COVID-19. Also, some media outlets and health systems have called for the discontinuation of these drugs in the context of suspected COVID-19. This has necessitated an urgent release of guidance on the use of such medications in COVID-19 patients. To date, multiple theories relating to the pure effects of renin-angiotensin-aldosterone system (RAAS) inhibitors on COVID-19 infections have been postulated. Favorable effects include blocking the ACE2 receptors, preventing viral entry into the heart and lungs, and protecting against lung injury in COVID-19. Adverse effects include a possible retrograde feedback mechanism that upregulates ACE2 receptors. This review provides greater insight into the role of the RAAS axis in acute lung injury and the effects of RAAS inhibitors on SARS-CoVs. The hypothesis that RAAS inhibitors facilitate viral insertion and the alternative hypothesis of the beneficial role of these drugs are discussed. Up-to-date published data concerning the RAAS inhibitors and COVID-19 are summarized.
Renin-Angiotensin-Aldosterone System (RAAS) Inhibitors and Coronavirus Disease 2019 (COVID-19)