Left ventricular hypertrophy does not prevent heart failure in experimental hypertension

HERNÁN GÓMEZ LLAMBÍ, H.; CAO, G.; DONATO, M.; SUÁREZ, D.; OTTAVIANO, G.; MÜLLER, A.; BUCHHOLZ, B.; GELPI, R.; OTERO-LOSADA, M.; MILEI, J.

INTERNATIONAL JOURNAL OF CARDIOLOGY

ELSEVIER IRELAND LTD

Año: 2017 vol. 238 p. 57 - 65

0167-5273

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