Figure 2.

Schematic diagram of the proposed role of the RAS in development of severe ARDS. In acute lung injury such as SARS-CoV infections, acid aspiration, pneumonias or sepsis, the generation of ANG II from ANG I is enhanced by ACE. ANG II contributes to acute lung failure through stimulation of the AT₁ receptor, whereas ACE2 and the AT₂ receptor negatively regulate this pathway and protect from acute lung failure. However, additional ACE2-regulated, but ANG II-independent, pathways seem to also contribute to ARDS.