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.
Keywords renin–angiotensin system - angiotensin - inflammation - coagulopathy - COVID-19
