Abstract
Coronary endothelial dysfunction leads to the increase in coronary blood flow and decrease in capillary density, and subsequently increases the incident of cardiac ischemia. Excess superoxide production (O2‐) has maladaptive effects on cellular functions in many tissues and organs. The objective of this study is to identify the role of O2‐ in coronary endothelial dysfunction in type 2 diabetic mice. Acetylcholine (ACh)‐induced relaxation (indicative of endothelium‐dependent relaxation) was significantly attenuated in diabetic coronary arteries (CAs) compared with control CAs. The pharmacological approach reveals that NO‐dependent relaxation, but not endothelial‐derived hyperpolarization‐dependent relaxation, is decreased in diabetic CAs. In the presence of Tempol (a O2‐scavenger), ACh‐induced relaxation in diabetic CAs is increased to the level seen in control CAs. In addition, mouse coronary endothelial cells (MCECs) isolated from diabetic mice exhibit significant increase in mitochondrial O2‐production and decrease in Mn‐SOD protein expression in comparison to those in control MCECs. These results suggest that the excess O2‐production in mitochondria attenuates the bioavailability of NO and subsequently decreases ACh‐induced relaxation in CAs in diabetic mice. This research was supported by grant DK083506.
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