ArticleJournal of molecular and cellular cardiology2015
Altered distribution of ICa impairs Ca release at the t-tubules of ventricular myocytes from failing hearts.
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 46 papers.
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Who cites it
46 citing papers in PubMed, 59 citations in OpenAlex.
- Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.Circulation research · 2026Article
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- A new approach to the determination of tubular membrane capacitance: passive membrane electrical properties under reduced electrical conductivity of the extracellular solution.Pflugers Archiv : European journal of physiology · 2022Article
- Fraction of the T-Tubular Membrane as an Important Parameter in Cardiac Cellular Electrophysiology: A New Way of Estimation.Frontiers in physiology · 2022Article
- A new model of myofibroblast-cardiomyocyte interactions and their differences across species.Biophysical journal · 2021Article
- Mechanisms and Regulation of Cardiac CaInternational journal of molecular sciences · 2021Review
- Mechanisms underlying pathological CaPflugers Archiv : European journal of physiology · 2021Review
- The role of calcium homeostasis remodeling in inherited cardiac arrhythmia syndromes.Pflugers Archiv : European journal of physiology · 2021Review
- Local hyperactivation of L-type CaScientific reports · 2021Article
- Nanoscale Study of Calcium Handling Remodeling in Right Ventricular Cardiomyocytes Following Pulmonary Hypertension.Hypertension (Dallas, Tex. : 1979) · 2021Article
- Beat-by-Beat Cardiomyocyte T-Tubule Deformation Drives Tubular Content Exchange.Circulation research · 2021Article
- Interaction of the Joining Region in Junctophilin-2 With the L-Type CaCirculation research · 2021Article
- Acute Detubulation of Ventricular Myocytes Amplifies the Inhibitory Effect of Cholinergic Agonist on Intracellular CaFrontiers in physiology · 2021Article
- The Physiology and Pathophysiology of T-Tubules in the Heart.Frontiers in physiology · 2021Review
- Nanoscale Organization, Regulation, and Dynamic Reorganization of Cardiac Calcium Channels.Frontiers in physiology · 2021Review
- Distinct features of calcium handling and β-adrenergic sensitivity in heart failure with preserved versus reduced ejection fraction.The Journal of physiology · 2020Article
- Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies.EBioMedicine · 2020Article
- Studying signal compartmentation in adult cardiomyocytes.Biochemical Society transactions · 2020Review
- Ivabradine and AF: Coincidence, Correlation or a New Treatment?Arrhythmia & electrophysiology review · 2020Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In mammalian cardiac ventricular myocytes, Ca influx and release occur predominantly at t-tubules, ensuring synchronous Ca release throughout the cell. Heart failure is associated with disrupted t-tubule structure, but its effect on t-tubule function is less clear. We therefore investigated Ca influx and release at the t-tubules of ventricular myocytes isolated from rat hearts ~18weeks after coronary artery ligation (CAL) or corresponding Sham operation. L-type Ca current (ICa) was recorded using the whole-cell voltage-clamp technique in intact and detubulated myocytes; Ca release at t-tubules was monitored using confocal microscopy with voltage- and Ca-sensitive fluorophores. CAL was associated with cardiac and cellular hypertrophy, decreased ejection fraction, disruption of t-tubule structure and a smaller, slower Ca transient, but no change in ryanodine receptor distribution, L-type Ca channel expression, or ICa density. In Sham myocytes, ICa was located predominantly at the t-tubules, while in CAL myocytes, it was uniformly distributed between the t-tubule and surface membranes. Inhibition of protein kinase A with H-89 caused a greater decrease of t-tubular ICa in CAL than in Sham myocytes; in the presence of H-89, t-tubular ICa density was smaller in CAL than in Sham myocytes. The smaller t-tubular ICa in CAL myocytes was accompanied by increased latency and heterogeneity of SR Ca release at t-tubules, which could be mimicked by decreasing ICa using nifedipine. These data show that CAL decreases t-tubular ICa via a PKA-independent mechanism, thereby impairing Ca release at t-tubules and contributing to the altered excitation-contraction coupling observed in heart failure.
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