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Related Experiment Video

Updated: Mar 28, 2026

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Benefits of Cardiac Resynchronization Therapy in an Asynchronous Heart Failure Model Induced by Left Bundle Branch Ablation and Rapid Pacing

Published on: December 11, 2017

Chronic therapy with α1A-adrenergic agonist reverses RV failure and mitochondrial dysfunction.

O Y Li¹, P M Swigart¹, N Reddy¹

¹Veterans Affairs Medical Center, San Francisco, and Department of Medicine, Univ. Calif. San Francisco, San Francisco.

Biorxiv : the Preprint Server for Biology

|March 27, 2026

Summary

Chronic treatment with an alpha1A-adrenergic receptor (α1A-AR) agonist reversed right ventricular failure (RVF) in mice. This therapeutic effect involved the reversal of mitochondrial dysfunction, suggesting α1A-AR as a target for RVF treatment.

Keywords:

ATP RV failure (RVF)mitochondria α1A-AR agonist therapy

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Last Updated: Mar 28, 2026

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Published on: December 11, 2017

Induction of Right Ventricular Failure by Pulmonary Artery Constriction and Evaluation of Right Ventricular Function in Mice

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Published on: May 13, 2019

Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension

Evaluation of Right Ventricular Function in Experimental Models of Pulmonary Arterial Hypertension

Published on: June 27, 2025

Area of Science:

Cardiology
Mitochondrial Biology
Pharmacology

Background:

Right ventricular failure (RVF) is a severe condition with high mortality and limited pharmacologic treatments.
Mitochondrial dysfunction is implicated in the pathophysiology of RVF, potentially impairing cardiomyocyte contractility via reduced ATP levels.

Purpose of the Study:

To investigate whether chronic treatment with an alpha1A-adrenergic receptor (α1A-AR) agonist improves mitochondrial function in a mouse model of RVF.
To determine if the reversal of RVF by α1A-AR agonist treatment is associated with enhanced mitochondrial function.

Main Methods:

A mouse model of RVF was induced by pulmonary artery constriction (PAC) for 2 weeks.
Mice with RVF were chronically treated with an α1A-AR agonist (A61603) or vehicle for an additional 2 weeks.
Right ventricular (RV) function was assessed by RV outflow tract fractional shortening (RVOT FS); mitochondrial respiration and ATP levels were measured.

Main Results:

PAC significantly reduced RVOT FS, RV myocardial respiration, and RV myocardial ATP levels.
Chronic A61603 treatment significantly improved RVOT FS compared to vehicle-treated PAC mice.
A61603 treatment also significantly increased RV myocardial respiration rate and RV myocardial ATP levels in PAC mice.

Conclusions:

Chronic α1A-AR agonist treatment reversed RVF in a mouse model.
The reversal of RVF was associated with improved mitochondrial function, including increased respiration and ATP levels.
These findings highlight the α1A-adrenergic receptor as a potential therapeutic target for RVF, acting through the enhancement of RV cardiomyocyte bioenergetic status.