Vascular Dysfunction in Fructose-Treated Mice is Associated with Increased Sensitivity to Angiotensin ii and Decreased to Nitric Oxide

Abstract High fructose consumption has been recognized as a potential risk factor for increased incidence of cardiovascular disease, and diabetes. Some lines of evidence support endothelial dysfunction (ED) as a possible underlying mechanism linking insulin resistance and hypertension. However, there is little information on the vascular response to vasoactive mediators after the high-fructose intaking (HFI). In this study, swiss mice had access to fructose-water solution (at 30% w/v) ad libitum for ten consecutive weeks. After this period, the vascular reactivity was assessed by the analyses of the variations in mean arterial pressure induced by either angiotensin II (Ang II) or sodium nitroprusside (SNP). Results showed that HFI induced i) an increased response to the vasoconstrictive and hypertensive agent Ang II, and ii) a decreased response to the vasodilating and hypotensive agent SNP. Western blot analysis revealed that such events were paralleled by higher Ang II type 1 receptor (AT1) and lower guanylate cyclase (GC-β1) enzyme densities in the mesenteric arterial bed (MAB). The present study demonstrated that HFI leads to an impaired response to vasoactive substances and, consequently, to ED in MAB.