Published online before print August 7, 2006, doi: 10.1161/01.HYP.0000237667.46006.f4
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(Hypertension. 2006;48:368.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
Extracellular Superoxide Dismutase Depletion in Hypertension Unmasks a New Role for Angiotensin II in Regulating Cu,Zn-Superoxide Dismutase Activity
From the Department of Physiology, New York Medical College, Valhalla, NY.
Correspondence to Michael S. Wolin, Department of Physiology, Basic Science Building, Rm 604, New York Medical College, Valhalla, NY 10595. E-mail mike_wolin@nymc.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
While studying the effects of 2 weeks of angiotensin II infusion in extracellular superoxide dismutase knockout (ecSOD–/–) mice on increasing superoxide and promoting hypertension, Gongora et al1 made the surprising observation that NO production and its associated endothelium-dependent relaxation were actually improved by angiotensin II treatment in aorta from these mice without altering the expression of endothelial NO synthase. The studies were initially designed to further examine in ecSOD–/– mice the concept that an elevation of superoxide causes a compensatory increase in the expression of ecSOD, which blunts the hypertensive response to angiotensin II and preserves endothelium-dependent vasodilatation. Evidence for this initial hypothesis was seen in measurements of blood pressure and in the response of isolated mesenteric resistance arteries. Angiotensin II treatment was observed to cause the hypothesized greater increase in blood pressure in the ecSOD–/– mice compared with control animals and a loss of endothelium-dependent relaxation to acetylcholine, associated with the detection of increased superoxide in the resistance arteries. Endothelium-dependent relaxation to acetylcholine was impaired in the aorta of ecSOD–/– mice even in the absence of angiotensin II treatment. Thus, a dominant effect of depleted ecSOD in resistance arteries and aorta is an attenuation of endothelium-dependent relaxation, which could originate from superoxide scavenging NO and/or impairment of the conversion of superoxide to hydrogen peroxide, a potential alternative mediator of endothelium-dependent relaxation in mouse mesenteric resistance arteries.2
The surprising observation made in the study by Gongora et al1 was that angiotensin II–elicited impairment of endothelium-dependent relaxation seen in control
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