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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:685.)
© 2006 American Heart Association, Inc.

Editorial

Mitochondrial Redox Control of Matrix Metalloproteinase Signaling in Resistance Arteries

Rhian M. Touyz

From the Kidney Research Centre, Ottawa Health Research Institute, University of Ottawa, Ontario, Canada.

Correspondence to Rhian M Touyz, MD, PhD, Canada Research Chair in Hypertension, Ottawa Health Research Institute, University of Ottawa, 451 Smyth Rd, Ottawa, ON, KIH 8M5. E-mail rtouyz@uottawa.ca

Key Words: reactive oxygen species • adrenergic receptors • transactivation • epidermal growth factor receptor • signal transduction • vascular tone

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

The importance of free radicals in the regulation of vascular tone was recognized in the late 1980s, when endothelium-derived relaxing factor was identified to be NO.^1,2 More recently, it has become clear that other free radicals, such as superoxide (O₂^–), hydrogen peroxide (H₂O₂), and peroxynitrite (ONOO-) also modulate vascular reactivity.^3,4 However, the exact role of reactive oxygen species (ROS) in the regulation of vascular contraction and relaxation remains elusive because vascular effects of free radicals are heterogeneous. Responses may differ depending on the species studied, the vascular bed under investigation, whether the endothelium is intact or denuded, and if studies are conducted in vitro or in vivo.^5,6 Furthermore, vascular actions of ROS may be direct or indirect and responses vary depending on the source of the free radicals and their site of compartmentalization.

See page 819

Superoxide has been implicated both as a vasoconstrictor and as a vasodilator. In cerebral vessels, low concentrations of O₂^–, generated by NADPH oxidase or xanthine oxidase, induce vasodilation.⁷ These effects may be mediated directly by activating potassium channels or indirectly through interactions with NO.⁸ On the other hand, high concentrations of O₂^– are potent vasoconstrictors, probably induced by ROS-stimulated increase in intracellular free Ca²⁺ concentration ([Ca²⁺]_i) or by increasing ONOO- production through interactions with NO.^9,10 The inactivation of NO by superoxide results in the loss of the vasodilator effect of NO, which, together with the direct contractile actions of ONOO-, leads to vasoconstriction. Similar biphasic dose-dependent responses have . . . [Full Text of this Article]

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