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1 Angiology, Institut de Recherches Servier, Suresnes, France
2 Department of Pharmacology, University of Hong Kong, Hong Kong, Hong Kong
* To whom correspondence should be addressed. E-mail: vanhoutt{at}hkucc.hku.hk.
Endothelial cells synthesize and release various factors that regulate angiogenesis, inflammatory responses, hemostasis as well as vascular tone and permeability. Endothelial dysfunction has been associated with a number of pathophysiological processes. Oxidative stress appears to be a common denominator underlying endothelial dysfunction in cardiovascular diseases. However, depending on the pathology, the vascular bed studied, the stimulant, and additional factors such as age, sex, salt intake, cholesterolemia, glycemia and hyperhomocysteinemia, the mechanisms underlying the endothelial dysfunction can be markedly different. A reduced bioavailability of nitric oxide (NO), an alteration in the production of prostanoids, including prostacyclin, thromboxane A2 and/or isoprostanes, an impairment of endothelium-dependent hyperpolarization as well as an increased release of endothelin-1 can individually or in association contribute to endothelial dysfunction. Therapeutic interventions do not necessarily restore a proper endothelial function and, when they do, may improve only part of these variables.
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