(Circulation. 1997;95:557-559.)
© 1997 American Heart Association, Inc.
Articles |
Oxidative Stress Produced by Angiotensin Too
Implications for Hypertension and Vascular Injury
the Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics, Iowa City.
Correspondence to Helgi J. Oskarsson, MD, Assistant Professor, Department of Internal Medicine, Division of Cardiovascular Diseases, University of Iowa Hospitals and Clinics, 200 Hawkins Dr, Iowa City, IA 52242. E-mail Helgi-Oskarsson@uiowa.edu.
Key Words: Editorials • endothelium-derived factors • hypertension • free radicals
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Introduction |
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Since the landmark study on renovascular hypertension by Goldblatt et al in 1934,1 it has become clear that the RAS plays a major role in hypertension and other cardiovascular disorders. Although the mechanism for RAS-induced hypertension is generally attributed to vasoconstrictor effects of angiotensin II and the salt- and water-retaining effects of aldosterone, a study by Bech Laursen et al in this issue of Circulation2 suggests an additional mechanism.
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Evidence That Angiotensin II Causes Hypertension via Production of Superoxide Radical |
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The study by Bech Laursen et al, coupled with their previous findings,3 suggests that angiotensin II–induced hypertension in rats is associated with a large increase in vascular production of superoxide radical, which is accompanied by impairment of EDNO-dependent vasodilation. This was not observed in rats made equally hypertensive by norepinephrine infusion.
The authors also observed that chronic infusion of liposome-encapsulated SOD increased conduit vessel SOD activity by 30%. This rather modest increase in SOD activity was nevertheless associated with normalization of superoxide release in the aorta from rats made hypertensive by angiotensin II, with restoration of normal EDNO-dependent vasorelaxation.
In addition, the authors showed that the development of hypertension in response to long-term infusion of angiotensin II was significantly inhibited by coadministration of liposome-encapsulated SOD, whereas the same treatment had no effect on hypertension induced by infusion of norepinephrine. Furthermore, rats with angiotensin II–induced hypertension that received liposome-encapsulated SOD showed a significantly greater reduction in mean arterial blood pressure in response to the endothelium-dependent vasodilator acetylcholine than did rats that were not treated with SOD. This suggests that SOD supplementation improves
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