Document Detail


Role of superoxide in angiotensin II-induced but not catecholamine-induced hypertension.
MedLine Citation:
PMID:  9024144     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The major source of superoxide (.O2-) in vascular tissues is an NADH/NADPH-dependent, membrane-bound oxidase. We have previously shown that this oxidase is activated in angiotensin II-but not norepinephrine-induced hypertension. We hypothesized that hypertension associated with chronically elevated angiotensin II might be caused in part by vascular .O2- production. METHODS AND RESULTS: We produced hypertension in rats by a 5-day infusion of angiotensin II or norepinephrine. Rats were also treated with liposome-encapsulated superoxide dismutase (SOD) or empty liposomes. Arterial pressure was measured in conscious rats under baseline conditions and during bolus injections of either acetylcholine or nitroprusside. Vascular .O2- production was assessed by lucigenin chemiluminescence. In vitro vascular relaxations were examined in organ chambers. Norepinephrine infusion increased blood pressure to a similar extent as angiotensin II infusion (179 +/- 5 and 189 +/- 4 mm Hg, respectively). In contrast, angiotensin II-induced hypertension was associated with increased vascular .O2- production, whereas norepinephrine-induced hypertension was not. Treatment with liposome-encapsulated SOD reduced blood pressure by 50 mm Hg in angiotensin II-infused rats while having no effect on blood pressure in control rats or rats with norepinephrine-induced hypertension. Similarly, liposome-encapsulated SOD enhanced in vivo hypotensive responses to acetylcholine and in vitro responses to endothelium-dependent vasodilators in angiotensin II-treated rats. CONCLUSIONS: Hypertension caused by chronically elevated angiotensin II is mediated in part by .O2-, likely via degradation of endothelium-derived NO. Increased vascular .O2- may contribute to vascular disease in high renin/angiotensin II states.
Authors:
J B Laursen; S Rajagopalan; Z Galis; M Tarpey; B A Freeman; D G Harrison
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Circulation     Volume:  95     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1997 Feb 
Date Detail:
Created Date:  1997-03-11     Completed Date:  1997-03-11     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  588-93     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Angiotensin II*
Animals
Aorta / pathology
Blood Pressure / drug effects
Blood Vessels / metabolism
Drug Carriers
Hypertension / chemically induced*,  pathology,  physiopathology*
Liposomes
Macrophages / pathology
Male
Nitroprusside / pharmacology
Norepinephrine*
Rats
Rats, Sprague-Dawley
Superoxide Dismutase / administration & dosage,  pharmacology
Superoxides / metabolism*
Vasodilation
Grant Support
ID/Acronym/Agency:
DK-45215/DK/NIDDK NIH HHS; HL-39006/HL/NHLBI NIH HHS; HL-48667/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Drug Carriers; 0/Liposomes; 11062-77-4/Superoxides; 11128-99-7/Angiotensin II; 15078-28-1/Nitroprusside; 51-41-2/Norepinephrine; 51-84-3/Acetylcholine; EC 1.15.1.1/Superoxide Dismutase
Comments/Corrections
Comment In:
Circulation. 1997 Feb 4;95(3):557-9   [PMID:  9024136 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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