Abstract 15033: Chronic Inhibition of Mitochondrial Reactive Oxygen Species Protects Against Endothelial SK Channel Dysfunction in Diabetes

• Published in: Circulation (New York, N.Y.) N.Y.), 2020-11, Vol.142 (Suppl_3 Suppl 3), p.A15033-A15033
• Main Authors: Xing, Hang, Zhang, Zhiqi, Song, Yi, shi, guangbin, Harrington, Elizabeth, Feng, Jun
• Format: Article
• Language: English
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/circ.142.suppl_3.15033

IntroductionOxidative stress plays an important role in the development of pathological condition in diabetes. Persistent oxidative stress during diabetes may result in impaired endothelium-independent vasodilation, by reducing small-conductance Ca2+-activated K+ (SK) channel activity. The mitochondria are main sources of reactive oxygen species (ROS) in diabetes, and mitochondria-targeted antioxidant mito-TEMPO (MT) prevents ROS generation has been found in a variety of disorders. However, few studies are available on the dysfunction of vasodilation and endothelial SK channels in diabetes after a chronic use of MT. PurposeWe investigated the chronic administration of MT on vasodilation in coronary arteries, and endothelial SK channel activity with or without diabetes. MethodsMT (1mg/kg) was applied to diabetic and health mice (n = 6/group) for 1 month. In-vitro relaxation response of pre-contracted arteries was examined in the presence or absence of the vasodilatory agents. Isolated endothelium was studied using whole-cell patch clamp recording SK channels currents. ResultsCoronary arteries dilation was decreased in diabetic mice compared with that in health (p