Document Detail

Allopurinol does not decrease blood pressure or prevent the development of hypertension in the deoxycorticosterone acetate-salt rat model.
MedLine Citation:
PMID:  20881613     Owner:  NLM     Status:  MEDLINE    
Reactive oxygen species play an important role in the pathogenesis of hypertension, disease in which reactive oxygen species levels and markers of oxidative stress are increased. Xanthine oxidase (XO) is a reactive oxygen species-producing enzyme the activity of which may increase during hypertension. Studies on XO inhibition effects on blood pressure have yielded controversial results. We hypothesized that XO inhibition would decrease blood pressure or attenuate the development of deoxycorticosterone acetate (DOCA)-salt hypertension. We administered the XO inhibitor, allopurinol (50 mg/kg per day, orally) or its vehicle to rats during the established or development stages of DOCA-salt hypertension. We validated XO inhibition by high-performance liquid chromatography measurements of XO metabolites in urine, serum, and tissues demonstrating a decrease in products, increase in substrates, and detection of the active metabolite of allopurinol, oxypurinol. We monitored blood pressure continuously through radiotelemetry and performed gross evaluations of target organs of hypertension. Allopurinol treatment did not impact the course of DOCA-salt hypertension regardless of the timing of administration. Aside from a significant decrease in pulse pressure in allopurinol-treated rats, no positive differences were observed between the allopurinol and the vehicle-treated rats. We conclude that XO does not play an important role in the development or maintenance of hypertension in the rat DOCA-salt hypertension model.
Theodora Szasz; A Elizabeth Linder; Robert P Davis; Robert Burnett; Gregory D Fink; Stephanie W Watts
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  56     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2011-04-21     Completed Date:  2012-02-14     Revised Date:  2014-09-08    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  627-34     Citation Subset:  IM    
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MeSH Terms
Allopurinol / pharmacology,  therapeutic use*
Blood Pressure / drug effects*,  physiology
Desoxycorticosterone / toxicity*
Disease Models, Animal*
Enzyme Inhibitors / pharmacology,  therapeutic use,  toxicity
Hypertension / chemically induced,  enzymology,  prevention & control*
Rats, Sprague-Dawley
Xanthine Oxidase / antagonists & inhibitors,  metabolism
Grant Support
P01 HL070687/HL/NHLBI NIH HHS; P01 HL070687-059002/HL/NHLBI NIH HHS; P01 HL70687/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Enzyme Inhibitors; 40GP35YQ49/Desoxycorticosterone; 63CZ7GJN5I/Allopurinol; EC Oxidase

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