Pathogenesis of ARDS
In addition to the classical views of ARDS including the
role of cellular and humoral mediators, the role of the
renin-angiotensin system (RAS) has been highlighted.
The RAS is thought to contribute to the pathophysiology
of ARDS by increasing vascular permeability.
Angiotensin-converting enzyme (ACE) is a key enzyme
of the RAS that converts inactive angiotensin I to the
vasoactive and aldosterone-stimulating peptide angiotensin
II and also metabolizes kinins along with many other
biologically active peptides. ACE is found in varying
levels on the surface of lung epithelial and endothelial cells [8]. Angiotensin II induces apoptosis of lung epithelial
and endothelial cells and is a potent fibrogenic
factor [9]. Based on these biological properties of ACE,
there is considerable interest in its potential involvement
in acute lung injury (ALI)/ARDS [10,11].