Renin-angiotensin-aldosterone system and COVID-19 infection
Fecha
2020Autor
Alexandre, Joachim
Cracowski, Jean-Luc
Richard, Vincent
Bouhanick, Béatrice
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Resumen
With the multiplication of COVID-19 severe acute respiratory syndrome cases due to SARS-COV2, some
concerns about angiotensin-converting enzyme 1 (ACE1) inhibitors (ACEi) and angiotensin II type 1
receptor blockers (ARB) have emerged. Since the ACE2 (angiotensin-converting enzyme 2) enzyme is
the receptor that allows SARS COV2 entry into cells, the fear was that pre-existing treatment with ACEi
or ARB might increase the risk of developing severe or fatal severe acute respiratory syndrome in case
of COVID-19 infection. The present article discusses these concerns. ACE2 is a membrane-bound enzyme
(carboxypeptidase) that contributes to the inactivation of angiotensin II and therefore physiologically
counters angiotensin II effects. ACEis do not inhibit ACE2. Although ARBs have been shown to up-regulate
ACE2 tissue expression in experimental animals, evidence was not always consistent in human studies.
Moreover, to date there is no evidence that ACEi or ARB administration facilitates SARS-COV2 cell entry
by increasing ACE2 tissue expression in either animal or human studies. Finally, some studies support
the hypothesis that elevated ACE2 membrane expression and tissue activity by administration of ARB
and/or infusion of soluble ACE2 could confer protective properties against inflammatory tissue damage
in COVID-19 infection. In summary, based on the currently available evidence and as advocated by many
medical societies, ACEi or ARB should not be discontinued because of concerns with COVID-19 infection,
except when the hemodynamic situation is precarious and case-by-case adjustment is required.
Palabras clave
COVID-19; Renin-angiotensin-aldosterone system; Arterial hypertensionEnlace al recurso
https://doi.org/10.1016/j.ando.2020.04.005Colecciones
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