ArticleJournal of molecular and cellular cardiology2015
Perturbed atrial calcium handling in an ovine model of heart failure: potential roles for reductions in the L-type calcium current.
Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Novel therapeutic cav1.3-C-terminus normalizes L-type calcium current and ejection fraction in ischemia-induced murine heart failure.Biochemical and biophysical research communications · 2025Article
- Maladaptive cardiomyocyte calcium handling in adult offspring of hypoxic pregnancy: protection by antenatal maternal melatonin.The Journal of physiology · 2024Article
- Restoring Atrial T-Tubules Augments Systolic Ca Upon Recovery From Heart Failure.Circulation research · 2024Article
- Increased Risk for Atrial Alternans in Rabbit Heart Failure: The Role of CaBiomolecules · 2023Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Role of CaArchives of toxicology · 2023Review
- Multi-Scale Computational Modeling of Spatial Calcium Handling From Nanodomain to Whole-Heart: Overview and Perspectives.Frontiers in physiology · 2022Review
- RyR2 and Calcium Release in Heart Failure.Frontiers in physiology · 2021Review
- Heart failure-induced atrial remodelling promotes electrical and conduction alternans.PLoS computational biology · 2020Article
- Remodeling Promotes Proarrhythmic Disruption of Calcium Homeostasis in Failing Atrial Myocytes.Biophysical journal · 2020Article
- Chronic vagal nerve stimulation has no effect on tachycardia-induced heart failure progression or excitation-contraction coupling.Physiological reports · 2020Article
- Calcium Buffering in the Heart in Health and Disease.Circulation · 2019Review
- Phosphodiesterase 5 inhibition improves contractile function and restores transverse tubule loss and catecholamine responsiveness in heart failure.Scientific reports · 2019Article
- Increased Vulnerability to Atrial Fibrillation Is Associated With Increased Susceptibility to Alternans in Old Sheep.Journal of the American Heart Association · 2018Article
- Runx1 Deficiency Protects Against Adverse Cardiac Remodeling After Myocardial Infarction.Circulation · 2018Article
- Reproducibility of science: Fraud, impact factors and carelessness.Journal of molecular and cellular cardiology · 2018Review
- Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure.Frontiers in physiology · 2018Review
- Increased Ca buffering underpins remodelling of CaThe Journal of physiology · 2017Article
- A computational model of spatio-temporal cardiac intracellular calcium handling with realistic structure and spatial flux distribution from sarcoplasmic reticulum and t-tubule reconstructions.PLoS computational biology · 2017Article
- Calcium and Excitation-Contraction Coupling in the Heart.Circulation research · 2017Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Heart failure (HF) is commonly associated with reduced cardiac output and an increased risk of atrial arrhythmias particularly during β-adrenergic stimulation. The aim of the present study was to determine how HF alters systolic Ca(2+) and the response to β-adrenergic (β-AR) stimulation in atrial myocytes. HF was induced in sheep by ventricular tachypacing and changes in intracellular Ca(2+) concentration studied in single left atrial myocytes under voltage and current clamp conditions. The following were all reduced in HF atrial myocytes; Ca(2+) transient amplitude (by 46% in current clamped and 28% in voltage clamped cells), SR dependent rate of Ca(2+) removal (kSR, by 32%), L-type Ca(2+) current density (by 36%) and action potential duration (APD90 by 22%). However, in HF SR Ca(2+) content was increased (by 19%) when measured under voltage-clamp stimulation. Inhibiting the L-type Ca(2+) current (ICa-L) in control cells reproduced both the decrease in Ca(2+) transient amplitude and increase of SR Ca(2+) content observed in voltage-clamped HF cells. During β-AR stimulation Ca(2+) transient amplitude was the same in control and HF cells. However, ICa-L remained less in HF than control cells whilst SR Ca(2+) content was highest in HF cells during β-AR stimulation. The decrease in ICa-L that occurs in HF atrial myocytes appears to underpin the decreased Ca(2+) transient amplitude and increased SR Ca(2+) content observed in voltage-clamped cells.
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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.