Cargando…
Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin
Early in the COVID-19 pandemic when it was first reported that SARS-CoV-2 used membrane-bound angiotensin-converting enzyme-2 (ACE2) as its receptor for entry into cells, warnings were raised against the use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) b...
Autores principales: | , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
2022
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696557/ https://www.ncbi.nlm.nih.gov/pubmed/36438606 |
_version_ | 1784838339480780800 |
---|---|
author | Speth, Robert C. Bader, Michael |
author_facet | Speth, Robert C. Bader, Michael |
author_sort | Speth, Robert C. |
collection | PubMed |
description | Early in the COVID-19 pandemic when it was first reported that SARS-CoV-2 used membrane-bound angiotensin-converting enzyme-2 (ACE2) as its receptor for entry into cells, warnings were raised against the use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) because of their potential to increase ACE2 expression. These reports ignored the adverse effects that the renin-angiotensin system (RAS) exerts on the cardiovascular system and kidneys via its primary hormone angiotensin (Ang) II acting upon AT(1) receptors that could exacerbate the cytokine storm induced by SARS-CoV-2 (1). At one point it was even recommended that COVID-19 patients suffering from cardiovascular collapse be administered Ang II to restore blood pressure rather than norepinephrine or vasopressin (2). An alternative strategy for treating COVID-19 was the administration of soluble ACE2 (sACE2) to act as a decoy receptor for the virus, misdirecting it away from vulnerable cells expressing membrane bound ACE2 (3–5). However, a paper published in early 2021 (6) described a scenario in which sACE2 and vasopressin played essential roles in SARS-CoV-2 infection of cells vulnerable to the virus. This commentary challenges both the (2) and (6) reports based upon their misconceptions and technical errors that pose a threat to the administration of life-saving therapies for severely affected COVID-19 patients. |
format | Online Article Text |
id | pubmed-9696557 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
record_format | MEDLINE/PubMed |
spelling | pubmed-96965572022-11-25 Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin Speth, Robert C. Bader, Michael Med Res Arch Article Early in the COVID-19 pandemic when it was first reported that SARS-CoV-2 used membrane-bound angiotensin-converting enzyme-2 (ACE2) as its receptor for entry into cells, warnings were raised against the use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) because of their potential to increase ACE2 expression. These reports ignored the adverse effects that the renin-angiotensin system (RAS) exerts on the cardiovascular system and kidneys via its primary hormone angiotensin (Ang) II acting upon AT(1) receptors that could exacerbate the cytokine storm induced by SARS-CoV-2 (1). At one point it was even recommended that COVID-19 patients suffering from cardiovascular collapse be administered Ang II to restore blood pressure rather than norepinephrine or vasopressin (2). An alternative strategy for treating COVID-19 was the administration of soluble ACE2 (sACE2) to act as a decoy receptor for the virus, misdirecting it away from vulnerable cells expressing membrane bound ACE2 (3–5). However, a paper published in early 2021 (6) described a scenario in which sACE2 and vasopressin played essential roles in SARS-CoV-2 infection of cells vulnerable to the virus. This commentary challenges both the (2) and (6) reports based upon their misconceptions and technical errors that pose a threat to the administration of life-saving therapies for severely affected COVID-19 patients. 2022-09 2022-09-20 /pmc/articles/PMC9696557/ /pubmed/36438606 Text en https://creativecommons.org/licenses/by/4.0/This is an open- access article distributed under the terms of the Creative Commons Attribution (https://creativecommons.org/licenses/by/4.0/) License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Article Speth, Robert C. Bader, Michael Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin |
title | Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin |
title_full | Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin |
title_fullStr | Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin |
title_full_unstemmed | Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin |
title_short | Why Angiotensin II is a Poor Choice for Circulatory Support of Ventilated COVID-19 Patients Compared to Vasopressin |
title_sort | why angiotensin ii is a poor choice for circulatory support of ventilated covid-19 patients compared to vasopressin |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9696557/ https://www.ncbi.nlm.nih.gov/pubmed/36438606 |
work_keys_str_mv | AT spethrobertc whyangiotensiniiisapoorchoiceforcirculatorysupportofventilatedcovid19patientscomparedtovasopressin AT badermichael whyangiotensiniiisapoorchoiceforcirculatorysupportofventilatedcovid19patientscomparedtovasopressin |