Abstract
Renin-angiotensin system (RAS) inhibition supposedly increases the expression of angiotensin converting enzyme 2, serving as a binding site for SARS-CoV-2. Concerns arose regarding therapy with RAS inhibition during the COVID-19 pandemic. However, the pharmacological restraining the classical RAS axis might be beneficial due to the reduction of deleterious effects of angiotensin II and enhancement of the anti-inflammatory angiotensin 1-7 pathway. Unless large controlled studies are performed, RAS inhibition remains the cornerstone therapy in populations with cardiovascular disorders.
MeSH terms
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Angiotensin II / blood
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Angiotensin II Type 1 Receptor Blockers / therapeutic use
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Angiotensin-Converting Enzyme 2
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Angiotensin-Converting Enzyme Inhibitors / therapeutic use
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Betacoronavirus / pathogenicity
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Betacoronavirus / physiology
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COVID-19
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Cardiovascular Diseases / complications
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Cardiovascular Diseases / drug therapy*
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Coronavirus Infections / complications*
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Coronavirus Infections / drug therapy
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Humans
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Pandemics
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Peptidyl-Dipeptidase A
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Pneumonia, Viral / complications*
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Pneumonia, Viral / drug therapy
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Renin-Angiotensin System*
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SARS-CoV-2
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Virus Internalization / drug effects
Substances
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Angiotensin II Type 1 Receptor Blockers
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Angiotensin-Converting Enzyme Inhibitors
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Angiotensin II
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Peptidyl-Dipeptidase A
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ACE2 protein, human
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Angiotensin-Converting Enzyme 2