Renin Angiotensin Aldosterone System Antagonism in 2019 Novel Coronavirus Acute Lung Injury

• Published in: Open forum infectious diseases Vol. 8; no. 10; p. ofab170
• Main Authors: Ventura, Davide, Carr, Amy L, Davis, R Duane, Silvestry, Scott, Bogar, Linda, Raval, Nirav, Gries, Cynthia, Hayes, Jillian E, Oliveira, Eduardo, Sniffen, Jason, Allison, Steven L, Herrera, Victor, Jennings, Douglas L, Page, Robert L, McDyer, John F, Ensor, Christopher R
• Format: Journal Article
• Language: English
• Published: US Oxford University Press 01.10.2021
• Subjects: Review; COVID-19; ACE2; SARS-CoV-2; angiotensin receptor blocker; ALI; ARDS; ACE inhibitor
• ISSN: 2328-8957; 2328-8957
• DOI: 10.1093/ofid/ofab170

Abstract It has been established that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) uses angiotensin-converting enzyme 2 (ACE2), a membrane-bound regulatory peptide, for host cell entry. Renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to increase ACE2 in type 2 pneumocyte pulmonary tissue. Controversy exists for the continuation of ACE inhibitors, angiotensin II receptor blockers, and mineralocorticoid receptor antagonists in the current pandemic. ACE2 serves as a regulatory enzyme in maintaining homeostasis between proinflammatory angiotensin II and anti-inflammatory angiotensin 1,7 peptides. Derangements in these peptides are associated with cardiovascular disease and are implicated in the progression of acute respiratory distress syndrome. Augmentation of the ACE2/Ang 1,7 axis represents a critical target in the supportive management of coronavirus disease 2019–associated lung disease. Observational data describing the use of RAAS inhibitors in the setting of SARS-CoV-2 have not borne signals of harm to date. However, equipoise persists, requiring an analysis of novel agents including recombinant human-ACE2 and existing RAAS inhibitors while balancing ongoing controversies associated with increased coronavirus infectivity and virulence.