| Role of Vascular Extracellular Superoxide Dismutase in Hypertension. | |
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MedLine Citation:
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PMID: 21730294 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Previous studies indicate that superoxide is important in the modulation of blood pressure but have not specifically identified the cell types or organs involved. We created mice with loxP sites flanking the extracellular superoxide dismutase (SOD3) gene. These mice were crossed with mice expressing inducible Cre-recombinase driven by the smooth muscle myosin heavy chain promoter allowing tissue-specific deletion of SOD3. Deletion of SOD3 increased vascular superoxide and reduced vascular NO levels as detected by electron spin resonance. Despite these changes in NO and superoxide, we did not observe increases in vascular inflammation caused by angiotensin II. Moreover, deletion of vascular SOD3 did not augment hypertension in response to angiotensin II. In additional studies, we also deleted SOD3 from the circumventricular organs by intracerebroventricular injection of an adenovirus encoding Cre-recombinase. Although this raised blood pressure and augmented the hypertension caused by angiotensin II, these responses were not further increased by vascular deletion of SOD3. These data suggest that the extracellular superoxide dismutase in vascular smooth muscle is not involved in the genesis of angiotensin II-induced hypertension and further emphasize the role of central SOD3 in the modulation of blood pressure. |
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Authors:
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Heinrich E Lob; Antony Vinh; Li Li; Yelena Blinder; Stefan Offermanns; David G Harrison |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-7-5 |
Journal Detail:
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Title: Hypertension Volume: - ISSN: 1524-4563 ISO Abbreviation: - Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-7-6 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA; Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany; Divisions of Clinical Pharmacology and Cardiology, Department of Internal Medicine, Vanderbilt University, Nashville, TN. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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