INTERRELATED REDOX-REGULATORY MECHANISMS BETWEEN THE SYMPATHOADRENAL SYSTEM AND ENDOTHELIAL DYSFUNCTION IN CORONARY ARTERY DISEASE

This article analyzes the interrelated molecular and redox-regulatory mechanisms between the sympathoadrenal system and endothelial dysfunction in coronary artery disease. Based on contemporary scientific evidence, the effects of chronic sympathetic hyperactivity induced by myocardial ischemia on the vascular endothelium, the reduction in nitric oxide bioavailability, the increased secretion of endothelin-1, and the enhancement of oxidative stress are discussed. The article also examines the complex pathophysiological interactions among reactive oxygen species, NADPH oxidase, uncoupled endothelial nitric oxide synthase, the renin–angiotensin–aldosterone system, and coronary microvascular dysfunction. In addition, the significance of malondialdehyde, one of the major products of lipid peroxidation, as a biomarker of oxidative stress is reviewed. The findings indicate that the interconnected pathological cycle involving sympathoadrenal activation, oxidative stress, and endothelial dysregulation represents one of the central mechanisms underlying the progression of coronary artery disease.