Document Detail


Role of vascular extracellular superoxide dismutase in hypertension.
MedLine Citation:
PMID:  21730294     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Heinrich E Lob; Antony Vinh; Li Li; Yelena Blinder; Stefan Offermanns; David G Harrison
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-07-05
Journal Detail:
Title:  Hypertension     Volume:  58     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2011 Aug 
Date Detail:
Created Date:  2011-07-21     Completed Date:  2011-09-28     Revised Date:  2014-09-18    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  232-9     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology
Animals
Aorta / metabolism*,  physiopathology
Blood Pressure / drug effects,  physiology*
Hydrogen Peroxide / metabolism
Hypertension / chemically induced,  genetics,  metabolism*,  physiopathology
Mice
Mice, Transgenic
Muscle, Smooth, Vascular / metabolism*,  physiopathology
Nitric Oxide / metabolism
Superoxide Dismutase / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
P01 HL058000/HL/NHLBI NIH HHS; P01 HL058000-10/HL/NHLBI NIH HHS; P01 HL058000-14/HL/NHLBI NIH HHS; P01HL058000/HL/NHLBI NIH HHS; P01HL095070/HL/NHLBI NIH HHS; R01 HL039006/HL/NHLBI NIH HHS; R01 HL039006-23/HL/NHLBI NIH HHS; R01HL039006/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
11128-99-7/Angiotensin II; 31C4KY9ESH/Nitric Oxide; BBX060AN9V/Hydrogen Peroxide; EC 1.15.1.1/Sod3 protein, mouse; EC 1.15.1.1/Superoxide Dismutase
Comments/Corrections

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