ArticleJCI insight2020
Cardiac sympathetic activation circumvents high-dose beta blocker therapy in part through release of neuropeptide Y.
Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
32 citing papers in PubMed, 47 citations in OpenAlex.
- Innervated human cardiac muscle model reveals sympathetic drivers of KCNH2-associated arrhythmias.Nature communications · 2026Article
- Article
- Targeting Neuropeptide Y: Novel Approaches to the Treatment of Cardiovascular and Haematological Disorders.Cardiovascular & hematological disorders drug targets · 2026Review
- Neural Regulation of Cardiac Arrhythmias: From the Brain-Heart Axis to Emerging Precision Therapies.Research (Washington, D.C.) · 2026Review
- Sympathovagal crosstalk: Y2-receptor blockade enhances vagal effects which in turn reduce NPY levels via muscarinic receptor activation.Cardiovascular research · 2025Article
- A novel approach to the prevention and management of cardiovascular diseases: targeting brain-heart axis.European journal of medical research · 2025Review
- Stellate Ganglia: A Key Therapeutic Target for Malignant Ventricular Arrhythmia in Heart Disease.Circulation research · 2025Review
- Targeted M-Channel Activation in the Left Stellate Ganglion Protects Against Ischemia-Induced Ventricular Arrhythmias in Canines.Journal of the American Heart Association · 2025Article
- Circulating noradrenaline leads to release of neuropeptide Y from cardiac sympathetic nerve terminals via activation of β-adrenergic receptors.The Journal of physiology · 2025Article
- Intravascular Sympathetic Stimulation to Facilitate Catheter Ablation of Premature Ventricular Complexes.JAMA cardiology · 2025Article
- Bioelectronic block of stellate ganglia mitigates pacing-induced heterogeneous release of catecholamine and neuropeptide Y in the infarcted pig heart.The Journal of physiology · 2025Article
- Bayliss Starling Prize Lecture 2023: Neuropeptide-Y being 'unsympathetic' to the broken hearted.The Journal of physiology · 2025Article
- Molecular and cellular neurocardiology in heart disease.The Journal of physiology · 2025Review
- The potential role of stellate ganglion block in impacting the central and peripheral systems: a narrative review.Frontiers in cardiovascular medicine · 2025Review
- Cardiac Sympathetic Innervation and Ventricular Arrhythmias in Structural Heart Disease: Current Peripheral Neuromodulation Therapies and Emerging Therapeutic Targets.Arrhythmia & electrophysiology review · 2025Review
- Non-invasive Neuromodulation of Arrhythmias.Cardiac electrophysiology clinics · 2024Review
- Antiarrhythmic Mechanisms of Epidural Blockade After Myocardial Infarction.Circulation research · 2024Article
- Article
- The adipose-neural axis is involved in epicardial adipose tissue-related cardiac arrhythmias.Cell reports. Medicine · 2024Article
- Management of patients with an electrical storm or clustered ventricular arrhythmias: a clinical consensus statement of the European Heart Rhythm Association of the ESC-endorsed by the Asia-Pacific Heart Rhythm Society, Heart Rhythm Society, and Latin-American Heart Rhythm Society.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The sympathetic nervous system plays an important role in the occurrence of ventricular tachycardia (VT). Many patients, however, experience VT despite maximal doses of beta blocker therapy, possibly due to the effects of sympathetic cotransmitters such as neuropeptide Y (NPY). The purpose of this study was to determine, in a porcine model, whether propranolol at doses higher than clinically recommended could block ventricular electrophysiological effects of sympathoexcitation via stellate ganglia stimulation, and if any residual effects are mediated by NPY. Greater release of cardiac NPY was observed at higher sympathetic stimulation frequencies (10 and 20 vs. 4 Hz). Despite treatment with even higher doses of propranolol (1.0 mg/kg), electrophysiological effects of sympathetic stimulation remained, with residual shortening of activation recovery interval (ARI), a surrogate of action potential duration (APD). Adjuvant treatment with the NPY Y1 receptor antagonist BIBO 3304, however, reduced these electrophysiological effects while augmenting inotropy. These data demonstrate that high-dose beta blocker therapy is insufficient to block electrophysiological effects of sympathoexcitation, and a portion of these electrical effects in vivo are mediated by NPY. Y1 receptor blockade may represent a promising adjuvant therapy to beta-adrenergic receptor blockade.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.