Effects of combined angiotensin II receptor antagonism and neprilysin inhibition in experimental pulmonary hypertension and right ventricular failure.


Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
15 10 2019
Historique:
received: 18 02 2019
revised: 03 06 2019
accepted: 24 06 2019
pubmed: 17 7 2019
medline: 10 7 2020
entrez: 17 7 2019
Statut: ppublish

Résumé

Combined angiotensin II receptor antagonism and neprilysin inhibition by LCZ696 reduces morbidity and mortality in heart failure patients and works by reducing RAAS activity and increasing cGMP levels. This study aims to evaluate the effects of LCZ696 in rats with pulmonary hypertension and right ventricular (RV) failure. Pulmonary hypertension was induced in rats (n = 34) by combined exposure to the vascular endothelial growth factor-receptor antagonist SU5416 and hypoxia (SuHx). To distinguish pulmonary vascular from cardiac effects, isolated RV failure was induced by pulmonary trunk banding (PTB) in another group of rats (n = 40). In both models, the development of RV dysfunction was verified before randomization to treatment with LCZ696 (60 mg/kg/day) or vehicle for five weeks. In the SuHx rats, LCZ696 treatment reduced the increase in RV pressure and the development of RV hypertrophy and RV dilatation compared with vehicle treatment. LCZ696 also reduced wall thickness of the smaller pulmonary arteries. In the PTB rats, LCZ696 treatment did not have any effects on RV hypertrophy or function. Combined angiotensin II receptor antagonism and neprilysin inhibition reduced RV systolic pressure, hypertrophy, and dilatation in rats with pulmonary hypertension. These effects seem secondary to pulmonary vascular changes, including reduced pulmonary vascular remodeling, as similar effects were not seen in rats with isolated RV failure. LCZ696 may have a therapeutic potential in the treatment of pulmonary hypertension.

Sections du résumé

BACKGROUND
Combined angiotensin II receptor antagonism and neprilysin inhibition by LCZ696 reduces morbidity and mortality in heart failure patients and works by reducing RAAS activity and increasing cGMP levels. This study aims to evaluate the effects of LCZ696 in rats with pulmonary hypertension and right ventricular (RV) failure.
METHODS
Pulmonary hypertension was induced in rats (n = 34) by combined exposure to the vascular endothelial growth factor-receptor antagonist SU5416 and hypoxia (SuHx). To distinguish pulmonary vascular from cardiac effects, isolated RV failure was induced by pulmonary trunk banding (PTB) in another group of rats (n = 40). In both models, the development of RV dysfunction was verified before randomization to treatment with LCZ696 (60 mg/kg/day) or vehicle for five weeks.
RESULTS
In the SuHx rats, LCZ696 treatment reduced the increase in RV pressure and the development of RV hypertrophy and RV dilatation compared with vehicle treatment. LCZ696 also reduced wall thickness of the smaller pulmonary arteries. In the PTB rats, LCZ696 treatment did not have any effects on RV hypertrophy or function.
CONCLUSIONS
Combined angiotensin II receptor antagonism and neprilysin inhibition reduced RV systolic pressure, hypertrophy, and dilatation in rats with pulmonary hypertension. These effects seem secondary to pulmonary vascular changes, including reduced pulmonary vascular remodeling, as similar effects were not seen in rats with isolated RV failure. LCZ696 may have a therapeutic potential in the treatment of pulmonary hypertension.

Identifiants

pubmed: 31307846
pii: S0167-5273(19)30876-9
doi: 10.1016/j.ijcard.2019.06.065
pii:
doi:

Substances chimiques

Aminobutyrates 0
Angiotensin II Type 2 Receptor Blockers 0
Antihypertensive Agents 0
Biphenyl Compounds 0
Drug Combinations 0
Tetrazoles 0
Valsartan 80M03YXJ7I
sacubitril and valsartan sodium hydrate drug combination WB8FT61183

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

203-210

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Stine Andersen (S)

Department of Cardiology, Aarhus University Hospital, Denmark. Electronic address: stineandersen@clin.au.dk.

Julie Birkmose Axelsen (JB)

Department of Cardiology, Aarhus University Hospital, Denmark.

Steffen Ringgaard (S)

MR Centre, Aarhus University Hospital, Denmark.

Jens Randel Nyengaard (JR)

Core Center for Molecular Morphology, Section for Stereology and Microscopy, Department of Clinical Medicine, Centre for Stochastic Geometry and Advanced Bioimaging, Aarhus University, Denmark.

Janus Adler Hyldebrandt (JA)

Department of Anesthesiology and Intensive Care, Aarhus University Hospital, Denmark.

Harm Jan Bogaard (HJ)

Department of Pulmonology, Amsterdam UMC, the Netherlands.

Frances S de Man (FS)

Department of Pulmonology, Amsterdam UMC, the Netherlands.

Jens Erik Nielsen-Kudsk (JE)

Department of Cardiology, Aarhus University Hospital, Denmark.

Asger Andersen (A)

Department of Cardiology, Aarhus University Hospital, Denmark.

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Classifications MeSH