As age-related reduction in ACh-induced vasorelaxation was ameliorated in GLO1 Tg rats without a change in vascular smooth muscle reactivity to NO, we speculated that GLO1 overexpression mitigated age-related endothelial dysfunction through increased net NO production by endothelium, or in other words NO bioavailability. This evidence concerns the gene GLO1 and endothelial dysfunction.