CC BY 4.0 · TH Open 2020; 04(02): e138-e144
DOI: 10.1055/s-0040-1713678
Review Article
Georg Thieme Verlag KG Stuttgart · New York

Pathological Role of Angiotensin II in Severe COVID-19

Wolfgang Miesbach
1   Department of Haemostaseology and Haemophilia Center, Institute of Transfusion Medicine, Medical Clinic 2, University Hospital Frankfurt, Frankfurt, Germany
› Author Affiliations
Further Information

Publication History

16 April 2020

19 May 2020

Publication Date:
26 June 2020 (online)

Abstract

The activated renin–angiotensin system induces a prothrombotic state resulting from the imbalance between coagulation and fibrinolysis. Angiotensin II is the central effector molecule of the activated renin–angiotensin system and is degraded by the angiotensin-converting enzyme 2 to angiotensin (1–7). The novel coronavirus infection (classified as COVID-19) is caused by the new coronavirus SARS-CoV-2 and is characterized by an exaggerated inflammatory response that can lead to severe manifestations such as acute respiratory distress syndrome, sepsis, and death in a proportion of patients, mostly elderly patients with preexisting comorbidities. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor to enter the target cells, resulting in activation of the renin–angiotensin system. After downregulating the angiotensin-converting enzyme 2, the vasoconstrictor angiotensin II is increasingly produced and its counterregulating molecules angiotensin (1–7) reduced. Angiotensin II increases thrombin formation and impairs fibrinolysis. Elevated levels were strongly associated with viral load and lung injury in patients with severe COVID-19. Therefore, the complex clinical picture of patients with severe complications of COVID-19 is triggered by the various effects of highly expressed angiotensin II on vasculopathy, coagulopathy, and inflammation. Future treatment options should focus on blocking the thrombogenic and inflammatory properties of angiotensin II in COVID-19 patients.