| PPARalpha stimulation exerts a blood pressure lowering effect through different mechanisms in a time-dependent manner. | |
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MedLine Citation:
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PMID: 19857485 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-10-24 |
Journal Detail:
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Title: European journal of pharmacology Volume: 627 ISSN: 1879-0712 ISO Abbreviation: Eur. J. Pharmacol. Publication Date: 2010 Feb |
Date Detail:
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Created Date: 2010-01-27 Completed Date: 2010-04-05 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1254354 Medline TA: Eur J Pharmacol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 185-93 Citation Subset: IM |
Copyright Information:
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Copyright (c) 2009 Elsevier B.V. All rights reserved. |
Affiliation:
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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. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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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:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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