The influence of 1-MNA on the vascular endothelium

Vascular endothelial dysfunction associated with lowered nitric oxide (NO) bioavailability inside vessels is an early and common mechanism leading to damage of blood vessels and as a consequence is a predisposition to cardiovascular incidents. Recent studies show that 1-MNA increases the bioavailability of NO in the vascular endothelium and hence regulates the impaired activity of endothelial nitric oxide synthase (Bartus et al., 2008, Domagala et al., 2012– Literature  >>).

Bartus et al. (Literature  >>) demonstrated that vasodilation in response to acetylcholine in animals with diabetes or hypertriglyceridemia is impaired (response depending on the endothelium and NO-induction). Chronic administration of 1-MNA to animals with hypertriglyceridemia resulted in vasodilation in these animals reverting back to the initial control level.

Diagram C. Influence of chronic 1-MNA administration (100 mg/kg) on aortic dilation in rats with hypertriglyceridemia - response to acetylcholine (depending on the endothelium) (Bartus et al., 2008Literature  >>)

These tests indicated that by increasing the bioavailability of nitric oxide, 1-MNA may prevent endothelial cell dysfunction, and it may restore proper endothelium function in cardiovascular disease (Domagala et al., 2012– Literature  >>). 1-MNA can reverse vascular endothelial dysfunction connected with impaired NO-dependent vasodilation (Bartus et al., 2008– Literature  >>).