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    
Abstract/OtherAbstract:
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.
Authors:
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.
Affiliation:
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
Descriptor/Qualifier:
Angiotensin II / metabolism
Animals
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
Male
Nitric Oxide Synthase Type III / metabolism
Oxidoreductases / metabolism
PPAR alpha / metabolism*
Rats
Rats, Wistar
Reactive Oxygen Species / metabolism
Receptors, Angiotensin / metabolism
Superoxide Dismutase / metabolism
Time Factors
Chemical
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 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.15.1.1/Superoxide Dismutase; EC 1.3.3.-/palmitoyl CoA oxidase

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