Endothelial nitric oxide synthase expression is
downregulated due to increased vascular ROS in COPD
Given that chronic CS exposure causes endothelium-dependent vascular
dysfunction, we then went on to investigate the potential underlying
mechanism driving this impaired vascular function. Endothelial
expression of the key vascular tone regulator eNOS and a marker of
oxidative stress, 3-nitrotyrosine (3-NT), were quantified. CS exposure
significantly reduced expression of eNOS by ~70%
(Figure 3A, p <0.05). In addition, the level of 3-NT
expression was significantly upregulated by ~3.2 fold
following CS exposure (Figure 3B, p<0.05 ), indicative
of enhanced vascular oxidative stress which may be responsible for the
reduced expression of eNOS.