tetano
Editor, Senior Moderator
Open Forum Infect Dis
. 2021 Apr 4;8(10)
fab170.
doi: 10.1093/ofid/ofab170. eCollection 2021 Oct.
Renin Angiotensin Aldosterone System Antagonism in 2019 Novel Coronavirus Acute Lung Injury
Davide Ventura[SUP] 1 [/SUP], Amy L Carr[SUP] 1 [/SUP], R Duane Davis[SUP] 2 [/SUP], Scott Silvestry[SUP] 2 [/SUP], Linda Bogar[SUP] 2 [/SUP], Nirav Raval[SUP] 2 [/SUP], Cynthia Gries[SUP] 2 [/SUP], Jillian E Hayes[SUP] 3 1 [/SUP], Eduardo Oliveira[SUP] 4 [/SUP], Jason Sniffen[SUP] 5 [/SUP], Steven L Allison[SUP] 3 1 [/SUP], Victor Herrera[SUP] 6 [/SUP], Douglas L Jennings[SUP] 7 8 [/SUP], Robert L Page 2nd[SUP] 9 [/SUP], John F McDyer[SUP] 10 [/SUP], Christopher R Ensor[SUP] 3 1 [/SUP]
Affiliations
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.
Keywords: ACE inhibitor; ACE2; ALI; ARDS; COVID-19; SARS-CoV-2; angiotensin receptor blocker.
. 2021 Apr 4;8(10)
fab170.doi: 10.1093/ofid/ofab170. eCollection 2021 Oct.
Renin Angiotensin Aldosterone System Antagonism in 2019 Novel Coronavirus Acute Lung Injury
Davide Ventura[SUP] 1 [/SUP], Amy L Carr[SUP] 1 [/SUP], R Duane Davis[SUP] 2 [/SUP], Scott Silvestry[SUP] 2 [/SUP], Linda Bogar[SUP] 2 [/SUP], Nirav Raval[SUP] 2 [/SUP], Cynthia Gries[SUP] 2 [/SUP], Jillian E Hayes[SUP] 3 1 [/SUP], Eduardo Oliveira[SUP] 4 [/SUP], Jason Sniffen[SUP] 5 [/SUP], Steven L Allison[SUP] 3 1 [/SUP], Victor Herrera[SUP] 6 [/SUP], Douglas L Jennings[SUP] 7 8 [/SUP], Robert L Page 2nd[SUP] 9 [/SUP], John F McDyer[SUP] 10 [/SUP], Christopher R Ensor[SUP] 3 1 [/SUP]
Affiliations
- PMID: 34642634
- PMCID: PMC8083494
- 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.
Keywords: ACE inhibitor; ACE2; ALI; ARDS; COVID-19; SARS-CoV-2; angiotensin receptor blocker.