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A healthy endothelium plays a central role in cardiovascular control. Therefore, endothelial dysfunction (ED), which is characterized by an imbalance between relaxing and contracting factors, procoagulant and anticoagulant substances, and between pro-inflammatory and anti-inflammatory mediators, may play a particularly significant role in the pathogenesis of atherosclerosis. ED is closely related to different risk factors of atherosclerosis, to their intensity and their duration. The involvement of risk factors in ED is also supported by results of intervention studies that showed regression of ED with treatment of risk factors. The common denominator whereby different risk factors cause ED is most probably increased oxidative stress and/or inflammation. ED promotes atherosclerosis and probably plays an important role in the development of thrombotic complications in the late stages of the disease. As ED is a key underlying factor in the atherosclerotic process, markers of endothelial abnormalities have been sought. Detection of ED is based on tests of endothelium-dependent vasomotion (dilation capability of peripheral and coronary arteries) and on circulating markers of endothelial function (endothelin-1, von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor, adhesion molecules). Using these tests it is possible to follow the dose-response of harmful effects or risk factors, and the effects of preventive procedures on vessel wall function.
[Int Angiol 2002;21:109-16]
Key words: Endothelium, vascular, physiology - Vasodilation - Atherosclerosis - Risk factors.
The vascular endothelium is an important regulatory organ in maintaining cardiovascular homeostasis. Normal endothelial function includes control over thrombosis and thrombolysis, platelets and leukocyte interaction with the vessel wall, and regulation of vascular tone and smooth muscle cell proliferation. One of the most important regulatory and vasoactive substances produced by endothelial cells is nitric oxide (NO). NO modulates vascular tone and inhibits the interaction between blood cells and the vessel wall. In addition NO appears to be an endogenous inhibitor of the bioactivity of the tumor necrosis factor, and the expression of pro-inflammatory molecules such as the vascular cell adhesion molecule (VCAM-1) and the chemoattractant protein-1 (MCP-1).1
Because the endothelium plays a central role in cardiovascular control, it follows that endothelial damage may contribute to disease states characterized by vasoconstriction, inflammation, excessive thrombus formation, leukocyte adhesion to vessel walls, as well as hypertension and atherosclerosis.2
Endothelial dysfunction
Endothelial dysfunction (ED) is characterized...