Regulation of Coronary Vasomotor Function by Reactive Oxygen Species

Overproduction of reactive oxygen species is closely associated with cardiovascular diseases in part by impairing endothelial function and consequently compromising blood flow regulation. Superoxide and hydrogen peroxide are elevated under various disease states with reduced endothelium-derived nitric oxide bioavailability. The oxidative stress elicited by angiotensin II, C-reactive protein and tumor necrosis factor-α is mediated by the activation of different redox signaling pathways in the microvasculature. The upregulation of L-arginine consuming enzyme arginase also contributes to the reduced nitric oxide bioavailability during oxidative stress. Hydrogen peroxide exhibits vasodilator function in the coronary microcirculation and plays an important role in the physiological regulation of coronary blood flow. However, excessive production of hydrogen peroxide impairs endothelial function by reducing L-arginine availability through hydroxyl radical-mediated upregulation of arginase. This review summarizes the current knowledge on the effects superoxide and hydrogen peroxide on vasomotor function regulated by the endothelium-derived nitric oxide and prostacyclin in the coronary microcirculation.