Discordance of endothelial nitric oxide synthase in the arterial wall and its circulating products in baboons: interactions with redox metabolism

BACKGROUND: Although peripheral arteries and circulating factors have been frequently used to assess systemic or central arterial, such as coronary artery, endothelial nitric oxide synthase (eNOS) functions, there is no direct evidence to support that they are related. DESIGN: We explored relationships in eNOS levels among coronary, aortic, carotid and brachial arteries, and interactions with redox metabolisms in 40 necropsied baboons (Papio hamadryas). RESULTS: We found no correlations in eNOS or NOx levels among all four arteries (R: 0.02-0.19, P > 0.05). While eNOS levels were high in both coronary (133.78 +/- 10.9 pg mg-1 protein) and aortic arteries (168.53 +/- 16.32 pg mg-1 protein), they were low in brachial (82.88 +/- 5.5 pg mg-1 protein) and carotid (89.83 +/- 7.15 pg mg-1 protein) arteries. Arterial eNOS were not correlated with plasma NOx either. However, coronary and aortic eNOS were positively correlated with the corresponding arterial total antioxidant status (TAS) (r = 0.638, P= 0.001, and r = 0.615, P= 0.0001). Coronary eNOS was also negatively associated with coronary advanced glycation end products (AGE) (r = -0.454, P= 0.003). Furthermore, there were significant associations in TAS levels between plasma and arterial wall extracts (R: 0.344-0.369, P < 0.05) and among arteries of different anatomic sites (R: 0.637-0.877, P < 0.001). While arterial TAS was negatively correlated with corresponding arterial AGE, TAS in the arterial wall and plasma were positively associated with plasma AGE. CONCLUSIONS: Our study shows that eNOS is differentially expressed in different anatomic sites and is not associated with plasma NOx, suggesting that brachial eNOS may not be used to assess coronary eNOS. The positive or negative associations between eNOS and TAS or AGE, especially in the coronary artery, indicate an important role of eNOS in arterial wall redox balance.