Figure 5.

RAAS and Bradykinin Systems in SAR-CoV-2 infection. SARS-CoV-2 infection results in interaction with transmembrane protease, serine 2 (TMPRSS2) and ACE2, leading to subsequent down regulation of ACE2 [27]. This loss of ACE2 function leads to decreased metabolism of Ang II to Ang(1-7) and Ang(1-9). This leads to an increased activation of AT₁R by Ang II and reduced activation of MasR. The resulting increased inflammation also leads to an increased expression of B₁Rs. As a consequence, AT₁R and B₁ receptor stimulation facilitates the pathophysiological responses associated with COVID-19, such as ARDS and CVCs (Figure adapted from [107]; created with Biorender.com).