Fig. 1.
Bradykinin signaling after SARS-CoV2 infection in pulmonary arterioles. Recent, high profile publications in eLife [4,5] have revealed that changes in the renin-angiotensin-aldosterone system after SARS-CoV2 infection could predispose bradykinin storms. Given that bradykinin and its metabolites are well-known inducers of endothelium-dependent vasodilation, vascular permeability, and pain via the activation of the G protein-coupled receptors B1 and B2, this signaling could be a novel therapeutic target in the treatment of COVID-19, including lung edema, cardiovascular dysfunction, and thromboembolism.