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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 3959087, 9 pages
Research Article

Angiotensin II-Induced Hypertension Is Attenuated by Overexpressing Copper/Zinc Superoxide Dismutase in the Brain Organum Vasculosum of the Lamina Terminalis

1Department of Veterinary and Biomedical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108, USA
2Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA

Received 14 September 2015; Accepted 30 November 2015

Academic Editor: Wei-Zhong Wang

Copyright © 2016 John P. Collister et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Angiotensin II (AngII) can access the brain via circumventricular organs (CVOs), including the subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT), to modulate blood pressure. Previous studies have demonstrated a role for both the SFO and OVLT in the hypertensive response to chronic AngII, yet it is unclear which intracellular signaling pathways are involved in this response. Overexpression of copper/zinc superoxide dismutase (CuZnSOD) in the SFO has been shown to attenuate the chronic hypertensive effects of AngII. Presently, we tested the hypothesis that elevated levels of superoxide () in the OVLT contribute to the hypertensive effects of AngII. To facilitate overexpression of superoxide dismutase, adenoviral vectors encoding human CuZnSOD or control adenovirus (AdEmpty) were injected directly into the OVLT of rats. Following 3 days of control saline infusion, rats were intravenously infused with AngII (10 ng/kg/min) for ten days. Blood pressure increased  mmHg in AdEmpty rats (), while rats overexpressing CuZnSOD () in the OVLT demonstrated a blood pressure increase of only  mmHg after 10 days of AngII infusion. These results support the hypothesis that overproduction of in the OVLT plays an important role in the development of chronic AngII-dependent hypertension.