ArticleLife sciences2020
Chronic heart failure increases negative chronotropic effects of adenosine in canine sinoatrial cells via A1R stimulation and GIRK-mediated I
Article in Life sciences, 2020. 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, 18 citations in OpenAlex.
- Increased GIRK channel activity prevents arrhythmia in mice with heart failure by enhancing ventricular repolarization.Scientific reports · 2023Article
- Sinus node dysfunction: current understanding and future directions.American journal of physiology. Heart and circulatory physiology · 2023Review
- Three-dimensional functional anatomy of the human sinoatrial node for epicardial and endocardial mapping and ablation.Heart rhythm · 2023Review
- Adenosine and Adenosine Receptors: Advances in Atrial Fibrillation.Biomedicines · 2022Review
- The Relevance of GIRK Channels in Heart Function.Membranes · 2022Review
- Ero1α-Dependent ERp44 Dissociation From RyR2 Contributes to Cardiac Arrhythmia.Circulation research · 2022Article
- Characterization of VU0468554, a New Selective Inhibitor of Cardiac G Protein-Gated Inwardly Rectifying KMolecular pharmacology · 2021Article
- Altered microRNA and mRNA profiles during heart failure in the human sinoatrial node.Scientific reports · 2021Article
- Pharmacologic Approach to Sinoatrial Node Dysfunction.Annual review of pharmacology and toxicology · 2021Review
- GPCR-dependent biasing of GIRK channel signaling dynamics by RGS6 in mouse sinoatrial nodal cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Inhibition of G protein-gated KScientific reports · 2020Article
- Genetic Ablation of G Protein-Gated Inwardly Rectifying KFrontiers in physiology · 2020Article
- Use of machine learning and Poincaré density grid in the diagnosis of sinus node dysfunction caused by sinoatrial conduction block in dogs.Journal of veterinary internal medicineArticle
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
aimsBradycardia contributes to tachy-brady arrhythmias or sinus arrest during heart failure (HF). Sinoatrial node (SAN) adenosine A1 receptors (ADO A1Rs) are upregulated in HF, and adenosine is known to exert negative chronotropic effects on the SAN. Here, we investigated the role of A1R signaling at physiologically relevant ADO concentrations on HF SAN pacemaker cells. MAIN
methodsDogs with tachypacing-induced chronic HF and normal controls (CTL) were studied. SAN tissue was collected for A1R and GIRK mRNA quantification. SAN cells were isolated for perforated patch clamp recordings and firing rate (bpm), slope of slow diastolic depolarization (SDD), and maximum diastolic potential (MDP) were measured. Action potentials (APs) and currents were recorded before and after addition of 1 and 10 μM ADO. To assess contributions of A1R and G protein-coupled Inward Rectifier Potassium Current (GIRK) to ADO effects, APs were measured after the addition of DPCPX (selective A1R antagonist) or TPQ (selective GIRK blocker). KEY
findingsA1R and GIRK mRNA expression were significantly increased in HF. In addition, ADO induced greater rate slowing and membrane hyperpolarization in HF vs CTL (p < 0.05). DPCPX prevented ADO-induced rate slowing in CTL and HF cells. The ADO-induced inward rectifying current, I SIGNIFICANCE: An increase in A1R and GIRK expression enhances I
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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.