| Pioglitazone treatment increases COX-2 derived PGI(2) production and reduces oxidative stress in hypertensive rats. Role on vascular function. | |
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MedLine Citation:
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PMID: 22220498 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Background and purpose: PPARγ agonists, glitazones, have cardioprotective and anti-inflammatory actions associated to gene transcription interference. This study analyzes if chronic treatment with pioglitazone of adult spontaneously hypertensive rats (SHR) alters blood pressure and vascular structure and function, and the possible mechanisms involved Experimental approach: Mesenteric resistance arteries from SHR untreated or pioglitazone-treated (2.5 mg.Kg(-1) .day(-1) , 28 days) and normotensive (WKY) rats were used. Vascular structure was studied by pressure myography, vascular function by wire myography, protein expression by western blot and immunohistochemistry, mRNA levels by RT-PCR, prostanoid levels by commercial kits and reactive oxygen species (ROS) production by dihydroethidium-emitted fluorescence. Key results: In SHR, pioglitazone treatment did not modify either blood pressure or vascular structural and mechanical alterations or phenylephrine-induced contraction, although it increased vascular COX-2 levels, PGI(2) production and the inhibitory effects of NS 398, SQ 29,548 and tranylcypromine on phenylephrine responses. The contractile phase of iloprost response, which was reduced by SQ 29,548, was greater in pioglitazone-treated and -untreated SHR than WKY. In addition, pioglitazone abolished the increased vascular ROS production, NOX-1 levels and the inhibitory effect of apocynin and allopurinol on phenylephrine contraction, while did not modify eNOS expression but restored the potentiatory effect of L-NAME on phenylephrine response. Conclusions and implications: Pioglitazone treatment, although did not reduce blood pressure in SHR, increased COX-2-derived PGI(2) production, reduced oxidative stress, and increased NO bioavailability, all of them involved on vasoconstrictor responses in resistance arteries. These effects would contribute to the cardioprotective effect of glitazones reported in several pathologies. |
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Authors:
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Raquel Hernanz; Angela Martín; Jose V Pérez-Girón; Roberto Palacios; Ana M Briones; Marta Miguel; Mercedes Salaices; María J Alonso |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-1-5 |
Journal Detail:
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Title: British journal of pharmacology Volume: - ISSN: 1476-5381 ISO Abbreviation: - Publication Date: 2012 Jan |
Date Detail:
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Created Date: 2012-1-6 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7502536 Medline TA: Br J Pharmacol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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© 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society. |
Affiliation:
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Depto. de Bioquímica, Fisiología y Genética Molecular, Universidad Rey Juan Carlos and Depto. de Farmacología, Universidad Autónoma de Madrid. |
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