ArticleThe Journal of physiology2007
Regulation of systolic [Ca2+]i and cellular Ca2+ flux balance in rat ventricular myocytes by SR Ca2+, L-type Ca2+ current and diastolic [Ca2+]i.
Article in The Journal of physiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Article
- The Mechanism of Modulation of Cardiac Force by Temperature.International journal of molecular sciences · 2025Article
- Observation of sarcomere chaos induced by changes in calcium concentration in cardiomyocytes.Biophysics and physicobiology · 2024Article
- Successful β-blocker introduction under intra-aortic balloon pumping and ivabradine in a patient with new-onset dilated cardiomyopathy and pulsus alternans: a case report.European heart journal. Case reports · 2024Article
- Ionic current changes underlying action potential repolarization responses to physiological pacing and adrenergic stimulation in adult rat ventricular myocytes.Physiological reports · 2023Article
- VDAC2 as a novel target for heart failure: CaCell calcium · 2022Review
- Effects of Sarcolemmal Background CaFrontiers in physiology · 2022Article
- Stress-dependent activation of myosin in the heart requires thin filament activation and thick filament mechanosensing.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Cx43 hemichannel microdomain signaling at the intercalated disc enhances cardiac excitability.The Journal of clinical investigation · 2021Article
- Nanoenviroments of the β-Subunit of L-Type Voltage-Gated Calcium Channels in Adult Cardiomyocytes.Frontiers in cell and developmental biology · 2021Article
- Visualization of Dynamic Mitochondrial Calcium Fluxes in Isolated Cardiomyocytes.Frontiers in physiology · 2021Article
- Calcium Dobesilate (CaD) Attenuates High Glucose and High Lipid-Induced Impairment of Sarcoplasmic Reticulum Calcium Handling in Cardiomyocytes.Frontiers in cardiovascular medicine · 2021Article
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Modulation of Calcium Transients in Cardiomyocytes by Transient Receptor Potential Canonical 6 Channels.Frontiers in physiology · 2020Article
- End-diastolic force pre-activates cardiomyocytes and determines contractile force: role of titin and calcium.The Journal of physiology · 2019Article
- The lack of slow force response in failing rat myocardium: role of stretch-induced modulation of Ca-TnC kinetics.The journal of physiological sciences : JPS · 2019Article
- Genetic background dominates the susceptibility to ventricular arrhythmias in a murine model of β-adrenergic stimulation.Scientific reports · 2018Article
- Ups and downs of calcium in the heart.The Journal of physiology · 2018Article
- Dynamic Action Potential Restitution Contributes to Mechanical Restitution in Right Ventricular Myocytes From Pulmonary Hypertensive Rats.Frontiers in physiology · 2018Article
- Calcium in the Pathophysiology of Atrial Fibrillation and Heart Failure.Frontiers in physiology · 2018Review
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The force-frequency response is an important physiological mechanism regulating cardiac output changes and is accompanied in vivo by beta-adrenergic stimulation. We sought to determine the role of sarcoplasmic reticulum (SR) Ca2+ content and L-type current (ICa-L) in the frequency response of the systolic Ca2+ transient alone and during beta-adrenergic stimulation. Experiments (on single rat ventricular myocytes) were designed to be as physiological as possible. Under current clamp stimulation SR Ca2+ content increased in line with stimulation frequency (1-8 Hz) but the systolic Ca2+ transient was maximal at 6 Hz. Under voltage clamp, increasing frequency decreased both systolic Ca2+ transient and ICa-L. Normalizing peak ICa-L by altering the test potential decreased the Ca2+ transient amplitude less than an equivalent reduction achieved through changes in frequency. This suggests that, in addition to SR Ca2+ content and ICa-L, another factor, possibly refractoriness of Ca2+ release from the SR contributes. Under current clamp, beta-adrenergic stimulation (isoprenaline, 30 nm) increased both the Ca2+ transient and the SR Ca2+ content and removed the dependence of both on frequency. In voltage clamp experiments, beta-adrenergic stimulation still increased SR Ca2+ content yet there was an inverse relation between frequency and Ca2+ transient amplitude and ICa-L. Diastolic [Ca2+]i increased with stimulation frequency and this contributed substantially (69.3 +/- 6% at 8 Hz) to the total Ca2+ efflux from the cell. We conclude that Ca2+ flux balance is maintained by the combination of increased efflux due to elevated diastolic [Ca2+]i and a decrease of influx on IC-L) on each pulse.
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