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BioMed Research International
Volume 2018, Article ID 2691014, 9 pages
https://doi.org/10.1155/2018/2691014
Research Article

Short-Term Treatment with Esmolol Reverses Left Ventricular Hypertrophy in Adult Spontaneously Hypertensive Rats via Inhibition of Akt/NF-κB and NFATc4

1Departamento de Anestesiología, Hospital General Universitario Gregorio Marañón, Doctor Esquero 46, 28007 Madrid, Spain
2Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain
3Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA 19140, USA
4Pfizer, CVMED, 610 Main Street, Cambridge, MA, USA
5Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain

Correspondence should be addressed to Begoña Quintana-Villamandos; moc.liamg@itniuqogeb

Received 28 October 2017; Revised 24 December 2017; Accepted 3 January 2018; Published 18 February 2018

Academic Editor: François Roubille

Copyright © 2018 Begoña Quintana-Villamandos et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Our group has previously demonstrated that short-term treatment with esmolol reduces left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHRs). The present study aimed to assess the molecular mechanisms related to this effect. Fourteen-month-old male were treated intravenously with saline as vehicle (SHR) or esmolol (SHR-E) (300 μg/kg/min). Age-matched vehicle-treated male Wistar-Kyoto (WKY) rats served as controls. After 48 hours of treatment, the hearts were harvested and left ventricular tissue was separated and processed for Western blot analysis to determine the levels of Akt, NF-κB, NFATc4, Creb1, Serca2a, Erk1/2, and Sapk/Jnk. Biomarkers of oxidative stress, such as catalase, protein carbonyls, total thiols, and total antioxidant capacity were evaluated. Esmolol reversed the levels of p-NFATc4, p-Akt, and p-NF-κB in SHRs to the phospholevels of these proteins in WKY rats without modifying p-Erk1/2, p-Sapk/Jnk, p-Creb1, or Serca2a in SHR. Compared with SHR, esmolol increased catalase activity and reduced protein carbonyls without modifying total thiols or total antioxidant capacity. Short-term treatment with esmolol reverses LVH in aged SHRs by downregulation of Akt/NF-κB and NFATc4 activity. Esmolol treatment also increases catalase activity and reduces oxidative stress in SHRs with LVH.