(Circulation. 2003;108:2054.)
© 2003 American Heart Association, Inc.
Mini-Review: Expert Opinions |
From the Department of Cardiac Surgery, University of Toronto, Toronto, Ontario, and Department of Pharmacology and Therapeutics, University of Calgary, Calgary, Alberta, Canada (S.V.); the Department of Pathology and Molecular Science, McMaster University, Health Sciences Centre, Hamilton, Ontario, Canada (M.B.); and the Department of Medicine, University of Calgary, Calgary, Alberta, Canada (T.J.A.).
Correspondence to Subodh Verma, MD, PhD, Division of Cardiac Surgery, 14EN-215, 200 Elizabeth St, Toronto General Hospital, Toronto, Ontario, Canada M5G 2C4. E-mail Subodh.Verma@Sympatico.ca
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Nitric oxide (NO) is the key endothelium-derived relaxing factor that plays a pivotal role in the maintenance of vascular tone and reactivity.2 In addition to being the main determinant of basal vascular smooth muscle tone, NO acts to negate the actions of potent endothelium-derived contracting factors such as angiotensin II and endothelin-1. In addition, NO serves to inhibit platelet and white cell activation and to maintain the vascular smooth muscle in a nonproliferative state. NO is synthesized from L-arginine under
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