Renin-angiotensin system and SARS-CoV-2 interaction: underlying mechanisms and potential clinical implications

Gen Physiol Biophys. 2020 May;39(3):203-204. doi: 10.4149/gpb_2020019.

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.

Publication types

  • Letter

MeSH terms

  • Angiotensin II / blood
  • Angiotensin II Type 1 Receptor Blockers / therapeutic use
  • Angiotensin-Converting Enzyme 2
  • Angiotensin-Converting Enzyme Inhibitors / therapeutic use
  • Betacoronavirus / pathogenicity
  • Betacoronavirus / physiology
  • COVID-19
  • Cardiovascular Diseases / complications
  • Cardiovascular Diseases / drug therapy*
  • Coronavirus Infections / complications*
  • Coronavirus Infections / drug therapy
  • Humans
  • Pandemics
  • Peptidyl-Dipeptidase A
  • Pneumonia, Viral / complications*
  • Pneumonia, Viral / drug therapy
  • Renin-Angiotensin System*
  • SARS-CoV-2
  • Virus Internalization / drug effects

Substances

  • Angiotensin II Type 1 Receptor Blockers
  • Angiotensin-Converting Enzyme Inhibitors
  • Angiotensin II
  • Peptidyl-Dipeptidase A
  • ACE2 protein, human
  • Angiotensin-Converting Enzyme 2