In vitro fructose exposure overactivates NADPH oxidase and causes oxidative stress in the isolated rat aorta

- Fructose in vitro exposure reduces sensitivity to acetylcholine on aortic segments.
- Fructose in vitro exposure increased response to phenylephrine on aorta.
- Fructose acute overload causes endothelium dysfunction on aorta.
- Fructose reduces nitric oxide modulation on aorta contractile responses.
- Fructose induces oxidative stress, possibly due to NADPH oxidase overactivation.

Fructose acutely interferes with cardiovascular function in humans and in animals, but the mechanisms remain unclear. Thus, we tested whether fructose can affect endothelial function without the interference of its metabolic effect by exposing the rat aorta to a high fructose concentration and then evaluate the vascular responses to vasoactive agents. We observed that fructose exposure causes overactivation of NADPH oxidase, which enhances superoxide anion production and increases NO degradation. Additionally, the enhanced vasoconstrictor action of hydrogen peroxide might exacerbate contractile responses. This vasoactive imbalance might be the key role by which fructose induces vascular dysfunction.