Papel de la quinasa regulada por suero y glucocorticoides 1 en las alteraciones cardiacas producidas por la aldosterona en ratas

  1. Martín Fernández, Beatriz
  2. Heras Jiménez, Natalia de las
  3. Valero, María
  4. Ballesteros, Sandra
  5. Cachofeiro Ramos, María Victoria
  6. Lahera Juliá, Vicente
Journal:
Clínica e investigación en arteriosclerosis

ISSN: 0214-9168 1578-1879

Year of publication: 2012

Volume: 24

Issue: 6

Pages: 267-274

Type: Article

More publications in: Clínica e investigación en arteriosclerosis

Metrics

SCImago Journal Rank

  • Year 2012
  • SJR Journal Impact: 0.133
  • Best Quartile: Q4
  • Area: Cardiology and Cardiovascular Medicine Quartile: Q4 Rank in area: 262/357
  • Area: Pharmacology (medical) Quartile: Q4 Rank in area: 197/274

Scopus CiteScore

  • Year 2012
  • CiteScore of the Journal : 0.2
  • Area: Pharmacology (medical) Percentile: 18
  • Area: Cardiology and Cardiovascular Medicine Percentile: 17

Abstract

Introduction: Aldosterone induces cardiac hypertrophy and it is known to induce serum and glucocorticoid regulated kinase 1 (SGK-1) gene expression. Aim: We aimed to evaluate structural, functional, inflammatory and oxidative alterations, as well as serum and glucocorticoid regulated kinase1 (SGK-1) expression, produced in rat heart by aldosterone + salt administration. Treatment with spironolactone was evaluated to prove mineralocorticoids mediation. Matherial and methods: Male Wistar rats received aldosterone (1 mg/kg/day) + 1% NaCl for 3 weeks. Half of the animals were treated with spironolactone (200 mg/kg/day). At the end of treatment hemodynamics were measured: SBP, DBP, LVEDP, LVSP, +dP/dt and �dP/dt. Heart relative weight was measured as cardiac hypertrophy index. mRNA expression of TGF-ß, CTGF, MMP2, TIMP2, TNF-a,IL-1ß, p22phox, eNOS and SGK-1 were measured. Cardiac collagen content was measured by histological techniques. Results: SBP and DBP, LVSP and LVEDP were elevated (P < .05) in aldosterone + salt-treated rats. �dP/dt decreased (P < .05) in aldosterone + salt-treated rats, but +dP/dt was similar in all groups. Spironolactone normalized (P < .05) SBP, DBP, LVSP, LVEDP and �dP/dt. Relative heart weight, collagen content, mRNA expression of TGF-ß, CTGF, MMP2, TIMP2, TNF-a, IL-1ß, p22phox, eNOS and SGK-1 were increased (P < .05) in aldosterone + salt-treated rats, being reduced by spironolactone (P < .05). Conlusions: SGK-1 might be a key mediator in the structural, functional and molecular cardiac alterations induced by aldosterone + salt in rats. All the observed changes and mediators are related with activation of mineralocorticoid receptors.