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REDUCED NO BIOAVAILABILITY, OXIDATIVE STRESS AND ALTERATION OF CALCIUM HOMEOSTASIS IN VASCULAR ENDOTHELIUM FROM DIABETIC MICE

Endothelial dysfunction is a major risk factor for vascular complications associated with diabetes. The purpose of this study was to evaluate the possible link between oxidative stress and alteration in calcium homeostasis in dysfunctional endothelial cells from db/db diabetic mice, 20 or 45 week old. Impaired flow‐induced dilation in mesenteric arteries and acetylcholine‐induced relaxation in aorta due to a decreased nitric oxide (NO) bioavailability were already shown in this model. For this study, mice aortic endothelial cells (MAEC) were isolated from vessel explants. Oxidative stress and Ca2+ homeostasis in MAEC were simultaneously recorded with DHE and Fura‐2 probes using an inverted epi‐fluorescence microscope. Compared to control mice, oxidative stress in MAEC from db/db mice increased with age leading to a progressive alteration of Ca2+ homeostasis, characterized by a rise in basal cytosolic calcium and a decrease in amplitude of acetylcholine‐induced calcium peak. Interestingly, a NO donor reduced oxidative stress and improved calcium signaling in endothelial cells from db/db mice. These results suggest that reduced NO bioavailability contributes to oxidative stress and abnormal calcium homeostasis in endothelial cells during progression of diabetes.