COVID-19 pathophysiology may be driven by an imbalance in the renin-angiotensin-aldosterone system

Abstract SARS-CoV-2 uses ACE2, an inhibitor of the Renin-Angiotensin-Aldosterone System (RAAS), for cellular entry. Studies indicate that RAAS imbalance worsens prognosis in COVID-19. We present a consecutive retrospective COVID-19 cohort with findings frequent pulmonary thromboembolism (17%), high artery pressure (60%) and lung MRI perfusion disturbances. demonstrate, swine, infusing angiotensin II or blocking ACE2 induces increased pressure, reduces blood oxygenation, increases coagulation, disturbs perfusion, diffuse alveolar damage, acute tubular necrosis compared to control animals. further demonstrate this imbalanced state can be ameliorated by infusion receptor blocker low-molecular-weight heparin. In work, we show pathophysiological swine induced shares several features clinical presentation. Therefore, propose severe could partially driven imbalance.