As we learn more about the pathophysiology of COVID-19, alternative treatments are being explored for the severe sequelae of this disease. SARS-CoV-2 enters human cells via the ACE2 receptor, located in many organs, including the heart, vascular endothelium, and alveolar epithelium causing an inflammatory cascade that can lead to ARDS, vasodilatory shock, myocarditis, acute kidney injury and capillary leak. Given the relationship between SARS-CoV-2 and the RAAS, is there a role for angiotensin II in vasodilatory shock caused by COVID-19?