Endothelial dysfunction: a multifaceted disorder (The Wiggers Award Lecture)

• Published in: American journal of physiology. Heart and circulatory physiology 2006-09, Vol.291 (3), p.H985-H1002
• Main Authors: Feletou, Michel, Vanhoutte, Paul M
• Format: Article
• Language: English
• Subjects: Animals; Atherosclerosis - etiology; Atherosclerosis - pathology; Atherosclerosis - physiopathology; Cardiovascular Diseases - etiology; Cardiovascular Diseases - pathology; Cardiovascular Diseases - physiopathology; Endothelin-1 - physiology; Endothelium, Vascular - pathology; Endothelium, Vascular - physiopathology; Hemostasis - physiology; Humans; Hypertension - complications; Hypertension - pathology; Hypertension - physiopathology; Inflammation - complications; Inflammation - pathology; Inflammation - physiopathology; Nitric Oxide - physiology; Oxidative Stress - physiology; Rats; Rats, Inbred SHR; Reactive Oxygen Species
• ISSN: 0363-6135; 1522-1539
• DOI: 10.1152/ajpheart.00292.2006

Department of Angiology, Institut de Recherches Servier, Suresnes, France and Department of Pharmacology, Faculty of Medicine, University of Hong Kong, Hong Kong, China 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 A 2 , 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. nitric oxide; prostaglandins; endothelium-derived hperpolarizing factor; endothelium-derived contracting factor; endothelin; oxidative stress; superoxide anion; hypertension; regenerated endothelium; angioplasty Address for reprint requests and other correspondence: P. M. Vanhoutte, Dept. of Pharmacology, 2/F, Laboratory Block, Faculty of Medicine Bldg., 21, Sassoon Rd., Pokfulam, Univ. of Hong Kong, Hong Kong, China (e-mail: vanhoutt{at}hkucc.hku.hk )