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Articles in PresS, published online ahead of print January 17, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00914.2001
Submitted on October 19, 2001
Accepted on January 14, 2002
1 Pharmacology, University of Saskatchewan, Saskatoon, Saskatchewan, Canada
2 Vascular Biology Unit, Boston University Medical Center, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: racohen{at}med-med1.bu.edu.
Our purpose was to address the role of NAPDH oxidase-derived superoxide anion in the vascular response to angiotensin (Ang) II. Blood pressure, aortic superoxide anion, 3-nitrotyrosine, and medial cross-sectional area were compared in wild type mice and in mice that over express human superoxide dismutase (hSOD). The pressor response to Ang II was significantly less in hSOD mice. Superoxide anion levels were increased 2-fold in Ang II-treated wild type mice, but not in hSOD mice. 3-nitrotyrosine increased in aortic endothelium and adventitia in wild type, but not in hSOD mice. In contrast, aortic medial cross-sectional area increased 50% with Ang II in hSOD mice, comparably to wild type mice. The lower pressor response to Ang II in the mice expressing hSOD is consistent with a pressor role of superoxide anion in wild type mice, most likely because it reacts with nitric oxide. Despite preventing the increase in superoxide anion and 3-nitrotyrosine, the aortic hypertrophic response to Ang II in vivo was unaffected by hSOD.
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