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(Circulation. 2006;113:1156-1158.)
© 2006 American Heart Association, Inc.

Editorial

Endothelin

Beyond a Vasoconstrictor

M. Gössl, MD; A. Lerman, MD

From the Division of Cardiovascular Diseases, Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minn.

Correspondence to Amir Lerman, MD, Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN 55905. E-mail lerman.amir@mayo.edu

Key Words: Editorials • endothelin • remodeling • coronary disease

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Almost 2 decades ago, endothelin-1 (ET-1) was identified as one of the most potent vasoconstrictors in the complex but well-balanced regulation of vascular tone.¹ Since then, through numerous clinical and experimental investigations, it has become evident that ET-1, beyond its function as a vasoactive peptide, also plays a seminal role in the atherogenic process by enhancing mitogenesis and inducing extracellular matrix formation. The role of ET-1 as an active participant in the atherogenic process is underscored by the observations that endothelin is highly and ubiquitously expressed in the extracellular space and the intracellular compartment (macrophages, myointimal cells, myofibroblasts, and endothelial cells) of human coronary atheromatous tissue.² Moreover, it has been demonstrated that circulating and tissue endothelin immunoreactivity correlates with the severity of human atherosclerotic disease.³ Taken together, these findings strongly suggest a major role for ET-1 in the evolution and progression of coronary atherosclerosis in humans. At the molecular level, nuclear factor-B, a key transcription factor of the inflammation-cascade, is activated by ET-1 in human monocytes,⁴ which further supports the role of ET-1 in the development of inflammation, a key feature of atherogenesis, within the vessel wall.

Article p 1180

Because of the development of endothelin antagonists suitable for experimental and human use, the functional role of ET-1 has been further elucidated. In experimental hypercholesterolemia, chronic endothelin receptor antagonism preserved coronary endothelial function and increased nitric oxide (NO) activity.⁵ Moreover, in the rodent atherosclerosis model, chronic ET_A receptor blockade not only normalized NO-mediated endothelial dysfunction but also significantly reduced . . . [Full Text of this Article]

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