Comparison of mechanisms involved in impaired vascular reactivity between high sucrose and high fat diets in rats

To determine the effects of high sucrose diets on vascular reactivity. We hypothesized that similar to high fat diets (HFD), HSD feeding would lead to increased adiposity resulting in inflammation and oxidative stress-mediated impairment of vasodilation.

Oxidative stress diminishes vasodilatory responsiveness in HSD and HFD rats through ROS-mediated scavenging of NO and decreased smooth muscle sensitivity to NO. Inflammation also plays a significant role in the impaired vasodilation.

Male Sprague-Dawley rats were fed control chow (Chow), HSD or HFD diets for 6 weeks. The role of inflammation and oxidative stress on impaired vasodilation were assessed in isolated mesenteric arterioles.

HSD and HFD induced increased adiposity, oxidative stress and inflammation. HFD rats developed fasting hyperglycemia. Both HSD and HFD rats developed impaired glucose tolerance and hyperleptinemia. Nitric oxide (NO)-mediated vasodilation was significantly attenuated in both HSD and HFD rats but was normalized by treatment with antioxidants or anti-inflammatory drugs. Endothelial NO synthase (eNOS) protein expression was not affected by diet. Sensitivity to NO was reduced since NOS inhibition attenuated vasodilation in Chow rats but did not further impair vasodilation in HSD or HFD rats. Likewise, responsiveness to a NO donor was attenuated in both experimental groups. Conclusions: Oxidative stress diminishes vasodilatory responsiveness in HSD and HFD rats through ROS-mediated scavenging of NO and decreased smooth muscle sensitivity to NO. Inflammation also plays a significant role in the impaired vasodilation.