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.