ArticlePloS one2012
Total beta-adrenoceptor knockout slows conduction and reduces inducible arrhythmias in the mouse heart.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- The beta1-adrenergic receptor in the heart.Cell death discovery · 2025Review
- Therapeutic Potential of the β3-Adrenergic Receptor and Its Ligands in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Fluoxetine promotes IL-10-dependent metabolic defenses to protect from sepsis-induced lethality.Science advances · 2025Article
- Association of Guideline-Based Medical Therapy with Malignant Arrhythmias and Mortality among Heart Failure Patients Implanted with Cardioverter Defibrillator (ICD) or Cardiac Resynchronization-Defibrillator Device (CRTD).Journal of clinical medicine · 2021Article
- Heart failure after pressure overload in autosomal-dominant desminopathies: Lessons from heterozygous DES-p.R349P knock-in mice.PloS one · 2020Article
- Increased arrhythmia susceptibility in type 2 diabetic mice related to dysregulation of ventricular sympathetic innervation.American journal of physiology. Heart and circulatory physiology · 2019Article
- Impact of Intracardiac Neurons on Cardiac Electrophysiology and Arrhythmogenesis in an Ex Vivo Langendorff System.Journal of visualized experiments : JoVE · 2018Article
- Overexpression of Cx43 in cells of the myocardial scar: Correction of post-infarct arrhythmias through heterotypic cell-cell coupling.Scientific reports · 2018Article
- Article
- Disruption of cardiac cholinergic neurons enhances susceptibility to ventricular arrhythmias.Nature communications · 2017Observational
- High fat diet induced alterations of atrial electrical activities in mice.American journal of cardiovascular disease · 2016Article
- β3-Adrenoceptor Impairs Mitochondrial Biogenesis and Energy Metabolism During Rapid Atrial Pacing-Induced Atrial Fibrillation.Journal of cardiovascular pharmacology and therapeutics · 2016Article
- let-7e replacement yields potent anti-arrhythmic efficacy via targeting beta 1-adrenergic receptor in rat heart.Journal of cellular and molecular medicine · 2014Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBeta-adrenoceptors (β-AR) play an important role in the neurohumoral regulation of cardiac function. Three β-AR subtypes (β(1), β(2), β(3)) have been described so far. Total deficiency of these adrenoceptors (TKO) results in cardiac hypotrophy and negative inotropy. TKO represents a unique mouse model mimicking total unselective medical β-blocker therapy in men. Electrophysiological characteristics of TKO have not yet been investigated in an animal model.
methodsIn vivo electrophysiological studies using right heart catheterisation were performed in 10 TKO mice and 10 129SV wild type control mice (WT) at the age of 15 weeks. Standard surface ECG, intracardiac and electrophysiological parameters, and arrhythmia inducibility were analyzed.
resultsThe surface ECG of TKO mice revealed a reduced heart rate (359.2±20.9 bpm vs. 461.1±33.3 bpm; p<0.001), prolonged P wave (17.5±3.0 ms vs. 15.1±1.2 ms; p = 0.019) and PQ time (40.8±2.4 ms vs. 37.3±3.0 ms; p = 0.013) compared to WT. Intracardiac ECG showed a significantly prolonged infra-Hisian conductance (HV-interval: 12.9±1.4 ms vs. 6.8±1.0 ms; p<0.001). Functional testing showed prolonged atrial and ventricular refractory periods in TKO (40.5±15.5 ms vs. 21.3±5.8 ms; p = 0.004; and 41.0±9.7 ms vs. 28.3±6.6 ms; p = 0.004, respectively). In TKO both the probability of induction of atrial fibrillation (12% vs. 24%; p<0.001) and of ventricular tachycardias (0% vs. 26%; p<0.001) were significantly reduced.
conclusionTKO results in significant prolongations of cardiac conduction times and refractory periods. This was accompanied by a highly significant reduction of atrial and ventricular arrhythmias. Our finding confirms the importance of β-AR in arrhythmogenesis and the potential role of unspecific beta-receptor-blockade as therapeutic target.
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