Another hypothesis states that SARS-CoV-2 infection blocks ACE2 function when binding to host cells, inhibiting its role of cleaving bradykinin and, as a consequence, bradykinin accumulates in the lung, promoting pulmonary edemas due to vasodilator activity and consequent respiratory failure. The increased bradykinin activation in the pulmonary endothelium can also induce neutrophil migration, enhancing tissue damage caused by the respiratory burst of these cells (88).