Literature DB >> 21262224

Aldosterone alters the participation of endothelial factors in noradrenaline vasoconstriction differently in resistance arteries from normotensive and hypertensive rats.

Fabiano E Xavier1, Javier Blanco-Rivero, María Soledad Avendaño, Esther Sastre, Rubén Yela, Kyra Velázquez, Mercedes Salaíces, Gloria Balfagón.   

Abstract

This study analyzed the effect of aldosterone (0.05mg/kg per day, 3 weeks) on vasoconstriction induced by noradrenaline in mesenteric resistance arteries from WKY rats and SHR. Contraction to noradrenaline was measured in mesenteric resistance arteries from untreated and aldosterone-treatedrats from both strains. Participation of nitric oxide (NO), superoxide anions, thromboxane A(2) (TxA(2)) and prostacyclin in this response was determined. 6-keto-prostaglandin (PG)F1alpha and thromboxane B(2) (TxB(2)) releases were determined by enzyme immunoassay. NO and superoxide anion release were also determined by fluorescence and chemiluminiscence, respectively. Aldosterone did not modify noradrenaline-induced contraction in either strain. In mesenteric resistance arteries from both aldosterone-treated groups, endothelium removal or preincubation with NO synthesis inhibitor L-NAME increased the noradrenaline-induced contraction, while incubation with the superoxide anion scavenger tempol decreased it. Preincubation with either the COX-1/2 or COX-2 inhibitor (indomethacin and NS-398, respectively) decreased the noradrenaline contraction in aldosterone-treated animals, while this response was not modified by COX-1 inhibitor SC-560. TxA(2) synthesis inhibitor (furegrelate), or TxA2 receptor antagonist (SQ 29 548) also decreased the noradrenaline contraction in aldosterone-treated animals. In untreated SHR, but not WKY rats, this response was increased by L-NAME, and reduced by tempol, indomethacin, NS-398 or SQ 29 548. Aldosterone treatment did not modify NO or TxB(2) release, but it did increase superoxide anion and 6-keto-PGF(1alpha) release in mesenteric resistance arteries from both strains. In conclusion, chronic aldosterone treatment reduces smooth muscle contraction to alpha-adrenergic stimuli, producing a new balance in the release of endothelium-derived prostanoids and NO.
Copyright © 2011. Published by Elsevier B.V.

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Year:  2011        PMID: 21262224     DOI: 10.1016/j.ejphar.2011.01.007

Source DB:  PubMed          Journal:  Eur J Pharmacol        ISSN: 0014-2999            Impact factor:   4.432


  7 in total

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Authors:  Sophocles Chrissobolis; Grant R Drummond; Frank M Faraci; Christopher G Sobey
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Authors:  Joana Beatriz Sousa; Maria Sofia Vieira-Rocha; Silvia M Arribas; Maria Carmen González; Paula Fresco; Carmen Diniz
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Authors:  Fernanda E Ramos-Alves; Diego B de Queiroz; Juliana Santos-Rocha; Gloria P Duarte; Fabiano E Xavier
Journal:  PLoS One       Date:  2012-11-28       Impact factor: 3.240

5.  Opposite effect of mast cell stabilizers ketotifen and tranilast on the vasoconstrictor response to electrical field stimulation in rat mesenteric artery.

Authors:  Esther Sastre; Laura Caracuel; Fabiano E Xavier; Gloria Balfagón; Javier Blanco-Rivero
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6.  Tranilast increases vasodilator response to acetylcholine in rat mesenteric resistance arteries through increased EDHF participation.

Authors:  Fabiano E Xavier; Javier Blanco-Rivero; Esther Sastre; Laura Caracuel; María Callejo; Gloria Balfagón
Journal:  PLoS One       Date:  2014-07-03       Impact factor: 3.240

7.  Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A.

Authors:  Pablo Llévenes; Raquel Rodrigues-Díez; Laia Cros-Brunsó; Mᵃ Isabel Prieto; Laura Casaní; Gloria Balfagón; Javier Blanco-Rivero
Journal:  Nutrients       Date:  2020-01-01       Impact factor: 5.717

  7 in total

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