ArticleInternational journal of molecular sciences2016
T-Tubular Electrical Defects Contribute to Blunted β-Adrenergic Response in Heart Failure.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- From function to structure: how myofibrillogenesis influences the transverse-axial tubular system development and its peculiarities.Frontiers in physiology · 2025Review
- Sex Differences in Mouse Cardiac Electrophysiology Revealed by Simultaneous Imaging of Excitation-Contraction Coupling.Journal of cardiovascular development and disease · 2023Article
- Cardiac sarcomere mechanics in health and disease.Biophysical reviews · 2021Review
- Review
- Recent progress in optical voltage-sensor technology and applications to cardiac research: from single cells to whole hearts.Progress in biophysics and molecular biology · 2020Review
- Review
- Interplay Between Sub-Cellular Alterations of Calcium Release and T-Tubular Defects in Cardiac Diseases.Frontiers in physiology · 2018Article
- New Insights in Cardiac Calcium Handling and Excitation-Contraction Coupling.Advances in experimental medicine and biology · 2018Review
- Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium.Frontiers in physiology · 2018Review
- Electrical defects of the transverse-axial tubular system in cardiac diseases.The Journal of physiology · 2017Review
- Quantitative assessment of passive electrical properties of the cardiac T-tubular system by FRAP microscopy.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Alterations of the β-adrenergic signalling, structural remodelling, and electrical failure of T-tubules are hallmarks of heart failure (HF). Here, we assess the effect of β-adrenoceptor activation on local Ca(2+) release in electrically coupled and uncoupled T-tubules in ventricular myocytes from HF rats. We employ an ultrafast random access multi-photon (RAMP) microscope to simultaneously record action potentials and Ca(2+) transients from multiple T-tubules in ventricular cardiomyocytes from a HF rat model of coronary ligation compared to sham-operated rats as a control. We confirmed that β-adrenergic stimulation increases the frequency of Ca(2+) sparks, reduces Ca(2+) transient variability, and hastens the decay of Ca(2+) transients: all these effects are similarly exerted by β-adrenergic stimulation in control and HF cardiomyocytes. Conversely, β-adrenergic stimulation in HF cells accelerates a Ca(2+) rise exclusively in the proximity of T-tubules that regularly conduct the action potential. The delayed Ca(2+) rise found at T-tubules that fail to conduct the action potential is instead not affected by β-adrenergic signalling. Taken together, these findings indicate that HF cells globally respond to β-adrenergic stimulation, except at T-tubules that fail to conduct action potentials, where the blunted effect of the β-adrenergic signalling may be directly caused by the lack of electrical activity.
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Registered trials
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