Related Experiment Video
Updated: Jul 27, 2026
A Model of Cardiac Remodeling Through Constriction of the Abdominal Aorta in Rats
Published on: December 2, 2016
Left ventricular hypertrophy does not prevent heart failure in experimental hypertension
H Hernán Gómez Llambí1, G Cao1, M Donato2
1Institute of Cardiological Research, School of Medicine, University of Buenos Aires, UBA-CONICET, Buenos Aires, Argentina.
Insights
Antihypertensive treatments may protect against heart failure (HF) by increasing thioredoxin expression, challenging the notion that left ventricular hypertrophy (LVH) is necessary for HF prevention.
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Hypertension-induced left ventricular hypertrophy (LVH) is paradoxically linked to increased cardiovascular risk.
- The role of LVH in preventing heart failure (HF) despite its association with adverse outcomes requires further investigation.
Purpose of the Study:
- To determine if antihypertensive medications inhibit LVH.
- To assess the impact of these treatments on beta-adrenergic response.
- To evaluate effects on myocardial oxidative metabolism.
Main Methods:
- Spontaneously hypertensive rats (SHR) received losartan, hydralazine, rosuvastatin, or carvedilol.
- Cardiac function was assessed using the Langendorff system with isoproterenol stimulation.
- Left ventricular weight and expression of key proteins (thioredoxin 1, peroxyredoxin 2, glutaredoxin 3, caspase-3, BNP) were measured.
Main Results:
- Antihypertensive treatments generally reduced blood pressure, though some groups showed elevated levels.
- Left ventricular weight normalized by body weight was increased in SHR and rosuvastatin groups.
- Expression of thioredoxin 1, peroxyredoxin 2, and glutaredoxin 3 was elevated across multiple treatment groups.
Conclusions:
- LVH may not be essential for preventing HF, contrary to traditional beliefs.
- Increased thioredoxin expression induced by antihypertensive therapy may contribute to HF protection.
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 16months, contractility was measured in 50% of rats (Langendorff system) before and after isoproterenol (Iso) 10-9M, 10-7M and 10-5M 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 (mmHg): 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 10-5M 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.
Related Concept Videos
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
01:20Mitral Regurgitation I: Introduction
01:29Heart Failure II: Pathophysiology
01:29Cardiomyopathy III: Hypertrophic Cardiomyopathy