NOS3 and endothelial dysfunction: As we have shown, eNOS S-glutathionylation is largely increased in GTN-treated endothelial cells and aortic tissue from GTN-infused rats, likely contributing to eNOS uncoupling and endothelial dysfunction in the setting of nitrate tolerance, which was largely prevented by AT1-receptor blocker therapy with telmisartan (Fig. 3) (Knorr et al, 2011).