Cardiovascular Research Advance Access originally published online on September 10, 2009
Cardiovascular Research 2009 84(2):178-179; doi:10.1093/cvr/cvp307
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.
Ascorbic acid and tetrahydrobiopterin: looking beyond nitric oxide bioavailability
Department of Physiology and Functional Genomics, University of Florida, PO Box 100274, 1600 SW Archer Road, Gainesville, FL 32610, USA
* Corresponding author. Tel: +1 352 392 3791; fax: +1 352 846 0270. E-mail address: jdelp@ufl.edu
This editorial refers to Ascorbic acid and tetrahydrobiopterin potentiate the EDHF phenomenon by generating hydrogen peroxide by A. Garry et al., pp. 218–226, this issue.
| The first 10% of the full text of this article appears below. |
Endothelial dysfunction, manifested as reduced vasodilatory capacity, occurs in arteries exposed chronically to cardiovascular risk factors.1 Hyperglycaemia, hypercholesterolaemia, hypertension, ageing, and smoking have all been associated with endothelial dysfunction.2–4 Although the molecular basis of endothelial dysfunction remains incompletely understood, numerous studies support a loss of bioavailable nitric oxide (NO) as a key mechanism underlying the dysfunction.1,4 Both tetrahydrobiopterin (BH4) and ascorbic acid play a role in sustaining NO bioavailabilty,5–7 and supplementation with either BH4 or ascorbic acid has been shown to improve endothelial function in humans and in animal models.6,8,9 As a result, investigations of the cardiovascular implications of treatment with exogenous BH4
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Cardiovasc Res 2009 84: 218-226.