Our research examines the role of nitric oxide in vascular homeostasis, particularly in neurovascular coupling and hemodynamic response in the brain and in exercise-induced functional hyperemia in skeletal muscle. In brain tissue, we focus on nitrite as an alternative source of nitric oxide and in the possibility of involvement of ascorbic acid in nitrite conversion to nitric oxide and importance of this process in neurovascular coupling. The second area of interest includes nitric oxide metabolism and the balance of NOx compounds (nitrite, nitrate, and RSNO) in the vasculature and tissues that are associated with limited oxygen supply during ischemia. We examine the possible use of NOx compounds in the prevention and treatment of reperfusion injury. Recently, our focus shifted to mammalian tissue nitrate and nitrite reductases as well as nonenzymatic nitrite reduction into nitric oxide and their importance in normal physiology and as a possible source of nitric oxide for exercise-induced hyperemia.