Vasomotor regulation of coronary microcirculation by oxidative stress: role of arginase.

摘要: Overproduction of reactive oxygen species, i.e., oxidative stress, is associated with the activation redox signaling pathways linking to inflammatory insults and cardiovascular diseases by impairing endothelial function consequently blood flow dysregulation due microvascular dysfunction. This review focuses on regulation vasomotor in coronary microcirculation nitric oxide (NO) during stress inflammation related L-arginine consuming enzyme arginase. Superoxide produced vascular wall compromises not only scavenging endothelium-derived NO but also inhibiting prostacyclin synthesis formation peroxynitrite. The upregulation arginase contributes deficiency dysfunction various initiating or following inflammation. Hydrogen peroxide, a diffusible stable oxidizing agent, exerts vasodilator plays important roles physiological flow. In occlusive ischemia, release hydrogen peroxide from microvasculature helps restore collateral microvessels exercise training. However, excessive production prolonged exposure impairs NO-mediated reducing availability through hydroxyl radical-dependent can be double-edged sword microcirculation, which tissue survival one way improving elicits injury other causing impact development angiotensin II receptor activation, hypertension, ischemia-reperfusion, hypercholesterolemia discussed.