Frontiers in Cardiovascular Medicine (Jun 2022)

Plasma Angiotensin II Is Increased in Critical Coronavirus Disease 2019

  • Rafael L. Camargo,
  • Bruna Bombassaro,
  • Milena Monfort-Pires,
  • Eli Mansour,
  • Andre C. Palma,
  • Luciana C. Ribeiro,
  • Raisa G. Ulaf,
  • Ana Flavia Bernardes,
  • Thyago A. Nunes,
  • Marcus V. Agrela,
  • Rachel P. Dertkigil,
  • Sergio S. Dertkigil,
  • Eliana P. Araujo,
  • Eliana P. Araujo,
  • Wilson Nadruz,
  • Wilson Nadruz,
  • Maria Luiza Moretti,
  • Licio A. Velloso,
  • Licio A. Velloso,
  • Andrei C. Sposito,
  • Andrei C. Sposito

DOI
https://doi.org/10.3389/fcvm.2022.847809
Journal volume & issue
Vol. 9

Abstract

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) employs angiotensin-converting enzyme 2 (ACE2) as its receptor for cell entrance, and studies have suggested that upon viral binding, ACE2 catalytic activity could be inhibited; therefore, impacting the regulation of the renin-angiotensin-aldosterone system (RAAS). To date, only few studies have evaluated the impact of SARS-CoV-2 infection on the blood levels of the components of the RAAS. The objective of this study was to determine the blood levels of ACE, ACE2, angiotensin-II, angiotensin (1–7), and angiotensin (1–9) at hospital admission and discharge in a group of patients presenting with severe or critical evolution of coronavirus disease 2019 (COVID-19). We showed that ACE, ACE2, angiotensin (1–7), and angiotensin (1–9) were similar in patients with critical and severe COVID-19. However, at admission, angiotensin-II levels were significantly higher in patients presenting as critical, compared to patients presenting with severe COVID-19. We conclude that blood levels of angiotensin-II are increased in hospitalized patients with COVID-19 presenting the critical outcome of the disease. We propose that early measurement of Ang-II could be a useful biomarker for identifying patients at higher risk for extremely severe progression of the disease.

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