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Structural, Functional, and Molecular Alterations Produced by Aldosterone Plus Salt in Rat Heart: Association With Enhanced Serum and Glucocorticoid–regulated Kinase-1 Expression

2010; Lippincott Williams & Wilkins; Volume: 57; Issue: 1 Linguagem: Inglês

10.1097/fjc.0b013e31820088ca

1533-4023

Beatriz Martín‐Fernández, Natalia de las Heras, María Miana, Sandra Ballesteros, Carmen Delgado, Su Song, Thomas H. Hintze, Victoria Cachofeiro, Vicente Lahera,

Eicosanoids and Hypertension Pharmacology

We aimed to evaluate the structural, functional, inflammatory, and oxidative alterations, as well as serum and glucocorticoid-regulated kinase-1 (SGK-1) expression, produced in rat heart by aldosterone + salt administration. Fibrosis mediators such as connective tissue growth factor, matrix metalloproteinase 2, and tissue inhibitor of metalloproteinases 2 were also evaluated. Treatment with spironolactone was evaluated to prove mineralocorticoid mediation. Male Wistar rats received aldosterone (1 mg·kg−1·d−1) + 1% NaCl for 3 weeks. Half of the animals were treated with spironolactone (200 mg·kg−1·d−1). Systolic and diastolic blood pressures, left ventricle (LV) systolic pressure, and LV end-diastolic pressure were elevated (P < 0.05) in aldosterone + salt-treated rats. In aldosterone + salt-treated rats, -dP/dt decreased (P < 0.05), but +dP/dt was similar in all groups. Spironolactone normalized (P < 0.05) systolic blood pressure, diastolic blood pressure, LV systolic pressure, LV end-diastolic pressure, and -dP/dt. Relative heart weight, collagen content, messenger RNA expression of transforming growth factor beta, connective tissue growth factor, matrix metalloproteinase 2, tissue inhibitor of metalloproteinases 2, tumor necrosis factor alpha, interleukin-1β, p22phox, endothelial nitric oxide synhtase, and SGK-1 were increased (P < 0.05) in aldosterone + salt-treated rats, being reduced by spironolactone (P < 0.05). 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 the activation of mineralocorticoid receptors.