Abstract
Angiotensin-converting enzyme (ACE) inhibitors (ACEIs) and angiotensin II type‑1 receptor blockers (ARBs) are among the most widely prescribed drugs for the treatment of arterial hypertension, heart failure and chronic kidney disease. A number of studies, mainly in animals and not involving the lungs, have indicated that these drugs can increase expression of angiotensin-converting enzyme 2 (ACE2). ACE2 is the cell entry receptor of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19) that is currently battering the globe. This has led to the hypothesis that use of ACEIs and ARBs may increase the risk of developing severe COVID-19. In this point of view paper, possible scenarios regarding the impact of ACEI/ARB pharmacotherapy on COVID-19 are discussed in relation to the currently available evidence. Although further research on the influence of blood-pressure-lowering drugs, including those not targeting the renin-angiotensin system, is warranted, there are presently no compelling clinical data showing that ACEIs and ARBs increase the likelihood of contracting COVID-19 or worsen the outcome of SARS-CoV‑2 infections. Thus, unless contraindicated, use of ACEIs/ARBs in COVID-19 patients should be continued in line with the recent recommendations of medical societies.
Highlights
In late December 2019, several clusters of pneumonia cases of unknown aetiology were reported in the city of Wuhan, People’s Republic of China
In the United States either ACE inhibitors (ACEIs) or angiotensin II type-1 receptor blockers (ARBs) are recommended in the first-line pharmacological treatment of HFrEF [15]
AngII/AngII type-1 receptor (AT1R) axis, which gained dominance due to severe acute respiratory syndrome (SARS)-CoV2-induced downregulation of angiotensin-converting enzyme 2 (ACE2) lung injury as determined by oxygenation index [18]. This led to the hypothesis that SARSCoV-2-mediated downregulation of ACE2 disturbs the balance between angiotensin-converting enzyme (ACE)/AngII/AT1R and ACE2/Ang1–7/ Mas receptor (MasR) signalling in the lungs and thereby contributes to the development of ARDS in COVID-19 patients (Fig. 2)
Summary
In late December 2019, several clusters of pneumonia cases of unknown aetiology were reported in the city of Wuhan, People’s Republic of China. The conversion of AngII into Ang1–7 by ACE2 reduces detrimental AngII/AT1R signalling and generates the ligand for the Mas receptor (MasR), activation of which opposes the effects of AT1R stimulation by AngII (Fig. 1).
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