ArticleAmerican journal of physiology. Heart and circulatory physiology2010
Ca2+ clock malfunction in a canine model of pacing-induced heart failure.
Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Chronic Partial Sleep Deprivation Increased the Incidence of Atrial Fibrillation by Promoting Pulmonary Vein and Atrial Arrhythmogenesis in a Rodent Model.International journal of molecular sciences · 2024Article
- Disruption of mitochondria-sarcoplasmic reticulum microdomain connectomics contributes to sinus node dysfunction in heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Heart failure in mice induces a dysfunction of the sinus node associated with reduced CaMKII signaling.The Journal of general physiology · 2022Article
- Slowing down as we age: aging of the cardiac pacemaker's neural control.GeroScience · 2022Review
- RyR2 and Calcium Release in Heart Failure.Frontiers in physiology · 2021Review
- Silencing miR-370-3p rescues funny current and sinus node function in heart failure.Scientific reports · 2020Article
- Heart Failure Differentially Modulates Natural (Sinoatrial Node) and Ectopic (Pulmonary Veins) Pacemakers: Mechanism and Therapeutic Implication for Atrial Fibrillation.International journal of molecular sciences · 2019Review
- Heart failure modulates electropharmacological characteristics of sinoatrial nodes.Experimental and therapeutic medicine · 2017Article
- Function and dysfunction of human sinoatrial node.Korean circulation journal · 2015Review
- Potential effects of intrinsic heart pacemaker cell mechanisms on dysrhythmic cardiac action potential firing.Frontiers in physiology · 2015Article
- Ca(2+) cycling properties are conserved despite bradycardic effects of heart failure in sinoatrial node cells.Frontiers in physiology · 2015Article
- Autonomic nerve activity and blood pressure in ambulatory dogs.Heart rhythm · 2014Article
- Heart failure decreases nerve activity in the right atrial ganglionated plexus.Journal of cardiovascular electrophysiology · 2012Article
- Abnormal response of superior sinoatrial node to sympathetic stimulation is a characteristic finding in patients with atrial fibrillation and symptomatic bradycardia.Circulation. Arrhythmia and electrophysiology · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The mechanisms of sinoatrial node (SAN) dysfunction in heart failure (HF) remain unclear. We hypothesized that impaired rhythmic spontaneous sarcoplasmic reticulum Ca(2+) release (Ca(2+) clock) plays an important role in SAN dysfunction in HF. HF was induced in canine hearts by rapid ventricular pacing. The location of pacemaking sites was determined in vivo using computerized electrical mapping in acute open-chest preparations (normal, n = 3; and HF, n = 4). Isoproterenol (Iso, 0.2 μg·kg(-1)·min(-1)) infusion increased heart rate and shifted the pacemaking site to the superior SAN in all normal hearts. However, in failing hearts, Iso did not induce superior shift of the pacemaking site despite heart rate acceleration. Simultaneous optical recording of intracellular Ca(2+) and membrane potential was performed in Langendorff-perfused isolated right atrium (RA) preparations from normal (n = 7) and failing hearts (n = 6). Iso increased sinus rate, enhanced late diastolic Ca(2+) elevation (LDCAE), and shifted the pacemaking sites to the superior SAN in all normal but in none of the HF RAs. Caffeine (2 ml, 20 mmol/l) caused LDCAE and increased heart rate in four normal RAs but in none of the three HF RAs. Iso induced ectopic beats from lower crista terminalis in five of six HF RAs. These ectopic beats were suppressed by ZD-7288, a specific pacemaker current (I(f)) blocker. We conclude that HF results in the suppression of Ca(2+) clock, resulting in the unresponsiveness of superior SAN to Iso and caffeine. HF also increases the ectopic pacemaking activity by activating the I(f) at the latent pacemaking sites in lower crista terminalis.
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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.