Document Detail

PPARalpha stimulation exerts a blood pressure lowering effect through different mechanisms in a time-dependent manner.
MedLine Citation:
PMID:  19857485     Owner:  NLM     Status:  MEDLINE    
Peroxisome proliferator activated receptors (PPARs) are a family of nuclear receptors that, upon activation with selective ligands, work as transcription factors. Recently, these have been related with the cardiovascular system. Our aim was to study PPARalpha-stimulation and its effects on blood pressure in rats with aortic coarctation, and to explore the role of the antioxidant system. Male Wistar rats (250-280 g) were distributed into the following groups: 1) sham; 2) aortic coarctated-vehicle-treated (AoCo-V), and 3) AoCo-clofibrate (100mg/kg) treated (AoCo-C). Rats were treated for 1 or 21 days. Clofibrate lowered blood pressure in both 1- and 21-day treatments. Renal reactive oxygen species increased after 1 day in AoCo-V, while clofibrate prevented this effect. Superoxide dismutase (SOD)-1 expression increased 3.6-fold upon PPARalpha stimulation (1 day) and returned to normal values by day 21. SOD-1 activity increased slightly in response to clofibrate. Renal activity of catalase increased in AoCo-C (1 day) and returned to normal (21 days). eNOS expression was not modified acutely (1 day) but increased at 21 days of treatment with clofibrate. Angiotensin II AT(1)-receptor expression as well as angiotensin II decreased in clofibrate-treated rats, while angiotensin II AT(2)-receptor expression increased, in both treatment periods. Angiotensin-(1-7) increased at 21 days. Our results suggest that in the early development of AoCo-induced hypertension, stimulation of PPARalpha increases the antioxidant defenses, leading to improvement in endothelial factors while in the sub-chronic phase (21 days), eNOS and angiotensin II receptors appear to play major roles in controlling blood pressure.
Luz Ibarra-Lara; Luz G Cervantes-P?rez; Francisca P?rez-Severiano; Leonardo Del Valle; Esther Rubio-Ru?z; Elizabeth Soria-Castro; Gustavo S Pastel?n-Hern?ndez; Mar?a S?nchez-Aguilar; Juan C Mart?nez-Lazcano; Alicia S?nchez-Mendoza
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-10-24
Journal Detail:
Title:  European journal of pharmacology     Volume:  627     ISSN:  1879-0712     ISO Abbreviation:  Eur. J. Pharmacol.     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-01-27     Completed Date:  2010-04-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1254354     Medline TA:  Eur J Pharmacol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  185-93     Citation Subset:  IM    
Copyright Information:
Copyright (c) 2009 Elsevier B.V. All rights reserved.
Department of Pharmacology, Instituto Nacional de Cardiolog?a Ignacio Ch?vez, Juan Badiano No. 1, Col. Secci?n XVI, Tlalpan, 14080 Mexico, D.F., Mexico City, Mexico.
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MeSH Terms
Angiotensin II / metabolism
Antioxidants / pharmacology
Aortic Coarctation / complications
Blood Pressure* / drug effects
Clofibrate / administration & dosage,  pharmacology
Gene Expression Regulation / drug effects
Hypertension / etiology,  metabolism,  physiopathology
Lipid Peroxidation / drug effects
Nitric Oxide Synthase Type III / metabolism
Oxidoreductases / metabolism
PPAR alpha / metabolism*
Rats, Wistar
Reactive Oxygen Species / metabolism
Receptors, Angiotensin / metabolism
Superoxide Dismutase / metabolism
Time Factors
Reg. No./Substance:
0/Antioxidants; 0/PPAR alpha; 0/Reactive Oxygen Species; 0/Receptors, Angiotensin; 11128-99-7/Angiotensin II; 637-07-0/Clofibrate; EC 1.-/Oxidoreductases; EC Oxide Synthase Type III; EC Dismutase; EC 1.3.3.-/palmitoyl CoA oxidase

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