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Artículo

Left ventricular hypertrophy does not prevent heart failure in experimental hypertension

Gómez Llambí de Oromí, Hernán Jorge; Cao, Gabriel FernandoIcon ; Donato, M.; Suárez, D.; Ottaviano, Graciela MabelIcon ; Müller, A.; Buchholz, BrunoIcon ; Gelpi, Ricardo JorgeIcon ; Otero-Losada, Matilde EstelaIcon ; Milei, JoseIcon
Fecha de publicación: 07/2017
Editorial: Elsevier Ireland
Revista: International Journal of Cardiology
ISSN: 0167-5273
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Patología

Resumen

Background Left ventricular hypertrophy (LVH) secondary to hypertension has been accepted to prevent heart failure (HF) while paradoxically increasing cardiovascular morbi-mortality. Objectives To evaluate whether antihypertensive treatment inhibits LVH, restores beta-adrenergic response and affects myocardial oxidative metabolism. Methods Ninety spontaneously hypertensive rats (SHR) were distributed into groups and treated (mg/kg, p.o.) with: losartan 30 (L), hydralazine 11 (H), rosuvastatin 10 (R), carvedilol 20 (C). Hypertension control group comprised 18 normotensive rats (Wistar-Kyoto, WKY). Following euthanasia at 16 months, contractility was measured in 50% of rats (Langendorff system) before and after isoproterenol (Iso) 10− 9 M, 10− 7 M and 10− 5 M stimulation. Left ventricular weight (LVW) was measured in the remaining hearts, and normalized by BW. Expression of thioredoxin 1 (Trx-1), peroxyredoxin 2 (Prx-2), glutaredoxin 3 (Grx-3), caspase-3 and brain natriuretic peptide (BNP) was determined. Results Systolic blood pressure (mm Hg): 154 ± 3 (L), 137 ± 1 (H), 190 ± 3 (R)*, 206 ± 3 (SHR)*, 183 ± 1 (C)**, and 141 ± 1 (WKY) (*p < 0.05 vs. L, H, WKY, **p < 0.05 vs. L, H, WKY, SHR). LVW/BW was higher in SHR and R (p < 0.05). Groups SHR, R and C evidenced baseline contractile depression. Response to Iso 10− 5 M was similar in WKY and L. Expression of Trx-1, Prx-2 and Grx-3 increased in C, H, R and L (p < 0.01). Conclusions Present findings argue against the traditional idea and support that LVH might not be required to prevent HF. Increased expression of thioredoxins by antihypertensive treatment might be involved in protection from HF.
Palabras clave: Bnp , Carvedilol , Caspase-3 , Grx-3 , Heart Failure , Hydralazine , Left Ventricular Hypertrophy , Losartan , Oxidative Stress , Prx-2 , Rosuvastatin , Trx-1
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info:eu-repo/semantics/openAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/41996
URL: https://www.sciencedirect.com/science/article/pii/S0167527317318636
DOI: http://dx.doi.org/10.1016/j.ijcard.2017.03.109
Colecciones
Articulos(ININCA)
Articulos de INST.DE INVEST.CARDIOLOGICAS (I)
Citación
Gómez Llambí de Oromí, Hernán Jorge; Cao, Gabriel Fernando; Donato, M.; Suárez, D.; Ottaviano, Graciela Mabel; et al.; Left ventricular hypertrophy does not prevent heart failure in experimental hypertension; Elsevier Ireland; International Journal of Cardiology; 238; 7-2017; 57-65
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