ArticleThe Journal of physiology2002
Mechanisms underlying the frequency dependence of contraction and [Ca(2+)](i) transients in mouse ventricular myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- Mechanisms underlying local CaThe Journal of physiology · 2025Article
- Physiology of intracellular calcium buffering.Physiological reviews · 2023Review
- Electrical and Structural Insights into Right Ventricular Outflow Tract Arrhythmogenesis.International journal of molecular sciences · 2023Review
- Effects of Cobra Cardiotoxins on Intracellular Calcium and the Contracture of Rat Cardiomyocytes Depend on Their Structural Types.International journal of molecular sciences · 2023Article
- L-type CaPhysiological reports · 2022Article
- Effects of Sarcolemmal Background CaFrontiers in physiology · 2022Article
- Two-variable nullcline analysis of ionic general equilibrium predicts calcium homeostasis in ventricular myocytes.PLoS computational biology · 2020Article
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Cardioprotection from stress conditions by weak magnetic fields in the Schumann Resonance band.Scientific reports · 2019Article
- Sources of CaJournal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2018Article
- Computational modeling of amylin-induced calcium dysregulation in rat ventricular cardiomyocytes.Cell calcium · 2018Article
- A modified approach for programmed electrical stimulation in mice: Inducibility of ventricular arrhythmias.PloS one · 2018Article
- Systolic [CaThe Journal of physiology · 2017Article
- Calcium and Excitation-Contraction Coupling in the Heart.Circulation research · 2017Review
- Computational analysis of the regulation of Ca(2+) dynamics in rat ventricular myocytes.Physical biology · 2015Article
- Redox regulation of cardiomyocyte cell cycling via an ERK1/2 and c-Myc-dependent activation of cyclin D2 transcription.Journal of molecular and cellular cardiology · 2015Article
- Tumor treating fields perturb the localization of septins and cause aberrant mitotic exit.PloS one · 2015Article
- Manganese Is Essential for Neuronal Health.Annual review of nutrition · 2015Review
- Calcium imaging at kHz frame rates resolves millisecond timing in neuronal circuits and varicosities.Biomedical optics express · 2014Article
- A novel computational model of mouse myocyte electrophysiology to assess the synergy between Na+ loading and CaMKII.The Journal of physiology · 2014Article
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
In most mammalian species force of contraction of cardiac muscle increases with increasing rate of stimulation, i.e. a positive force-frequency relationship. In single mouse ventricular cells, both positive and negative relationships have been described and little is known about the underlying mechanisms. We studied enzymatically isolated single ventricular mouse myocytes, at 30 degrees C. During field stimulation, amplitude of unloaded cell shortening increased with increasing frequency of stimulation (0.04 +/- 0.01 Delta L/L(0) at 1 Hz to 0.07 +/- 0.01 Delta L/L(0) at 4 Hz, n = 12, P < 0.05). During whole cell voltage clamp with 50 microM [K5-fluo-3](pip), both peak and baseline [Ca(2+)](i) increased at higher stimulation frequencies, but the net Delta[Ca(2+)](i) increased only modestly from 1.59 +/- 0.08 Delta F/F(0) at 1 Hz, to 1.71 +/- 0.11 Delta F/F(0) at 4 Hz (n = 17, P < 0.05). When a 1 s pause was interposed during stimulation at 2 and 4 Hz, [Ca(2+)](i) transients were significantly larger (at 4 Hz, peak F/F(0) increased by 78 +/- 2 %, n = 5). SR Ca(2+) content assessed during caffeine application, significantly increased from 91 +/- 24 micromol l(-1) at 1 Hz to 173 +/- 20 micromol l(-1) at 4 Hz (n = 5, P < 0.05). Peak I(Ca,L) decreased at higher frequencies (by 28 +/- 6 % at 2 Hz, and 45 +/- 8 % at 4 Hz), due to slow recovery from inactivation. This loss of I(Ca,L) resulted in reduced fractional release. Thus, in mouse ventricular myocytes the [Ca(2+)](i)-frequency response depends on a balance between the increase in SR content and the loss of trigger I(Ca,L). Small changes in this balance may contribute to variability in frequency-dependent behaviour. In addition, there may be a regulation of the contractile response downstream of [Ca(2+)](i).
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