Modulation of vascular function by AMPK: Assessment of NO bioavailability and surrogates of oxidative stress

Abstract

The endothelium plays a pivotal role in the development of vascular disease. Decreased bioavailability of nitric oxide, a condition known as “endothelial dysfunction,” is considered an early step in this process before atherosclerotic changes of the vessel wall occur. Endothelium-derived nitric oxide (•NO) may be rapidly scavenged by superoxide anions; therefore, the equilibrium between •NO production on one hand and its inactivation by oxidative stress on the other hand is of particular interest. Metabolic enzyme systems such as AMP-activated protein kinase (AMPK) may affect the cellular production of •NO or reactive oxygen species (ROS), while AMPK activity itself can also be modulated by ROS. Therefore, the analysis of •NO as well as ROS levels is essential to understand how metabolism regulating enzymes like AMPK may modulate vascular disease.