ArticleThe Journal of physiology2000
Modulation of CICR has no maintained effect on systolic Ca2+: simultaneous measurements of sarcoplasmic reticulum and sarcolemmal Ca2+ fluxes in rat ventricular myocytes.
Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 166 citations in OpenAlex.
- Using a Failing Human Ventricular Cardiomyocyte Model to Re-Evaluate CaBiomolecules · 2024Article
- Preserved cardiac performance and adrenergic response in a rabbit model with decreased ryanodine receptor 2 expression.Journal of molecular and cellular cardiology · 2022Article
- CaPflugers Archiv : European journal of physiology · 2022Review
- Cx43 hemichannel microdomain signaling at the intercalated disc enhances cardiac excitability.The Journal of clinical investigation · 2021Article
- Determinants of Ca2+ release restitution: Insights from genetically altered animals and mathematical modeling.The Journal of general physiology · 2020Article
- Atrial Myocyte NLRP3/CaMKII Nexus Forms a Substrate for Postoperative Atrial Fibrillation.Circulation research · 2020Article
- Region-specific mechanisms of corticosteroid-mediated inotropy in rat cardiomyocytes.Scientific reports · 2020Article
- The Control of Diastolic Calcium in the Heart: Basic Mechanisms and Functional Implications.Circulation research · 2020Review
- Novel approach for quantification of endoplasmic reticulum CaAmerican journal of physiology. Heart and circulatory physiology · 2019Article
- Calcium Buffering in the Heart in Health and Disease.Circulation · 2019Review
- Activation of CaMKIIδA promotes CaActa pharmacologica Sinica · 2018Article
- NCX-Mediated Subcellular CaBiophysical journal · 2018Article
- Runx1 Deficiency Protects Against Adverse Cardiac Remodeling After Myocardial Infarction.Circulation · 2018Article
- Ups and downs of calcium in the heart.The Journal of physiology · 2018Article
- Systolic [CaThe Journal of physiology · 2017Article
- Calcium and Excitation-Contraction Coupling in the Heart.Circulation research · 2017Review
- Sarcolemmal distribution ofAmerican journal of physiology. Heart and circulatory physiology · 2017Article
- Gene Therapy With Angiotensin-(1-9) Preserves Left Ventricular Systolic Function After Myocardial Infarction.Journal of the American College of Cardiology · 2016Article
- Biphasic decay of the Ca transient results from increased sarcoplasmic reticulum Ca leak.The Journal of physiology · 2016Article
- Late Na(+) current and protracted electrical recovery are critical determinants of the aging myopathy.Nature communications · 2015Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of modulating Ca2+-induced Ca2+ release (CICR) in single cardiac myocytes were investigated using low concentrations of caffeine (< 500 microM) in reduced external Ca2+ (0.5 mM). Caffeine produced a transient potentiation of systolic [Ca2+]i (to 800 % of control) which decayed back to control levels. 2. Caffeine decreased the steady-state sarcoplasmic reticulum (SR) Ca2+ content. As the concentration of caffeine was increased, both the potentiation of the systolic Ca2+ transient and the decrease in SR Ca2+ content were increased. At higher concentrations, the potentiating effect decayed more rapidly but the rate of recovery on removal of caffeine was unaffected. 3. A simple model in which caffeine produces a fixed increase in the fraction of SR Ca2+ which is released could account qualitatively but not quantitatively for the above results. 4. The changes in total [Ca2+] during systole were obtained using measurements of the intracellular Ca2+ buffering power. Caffeine initially increased the fractional release of SR Ca2+. This was followed by a decrease to a level greater than that under control conditions. The fraction of systolic Ca2+ which was pumped out of the cell increased abruptly upon caffeine application but then recovered back to control levels. The increase in fractional loss is due to the fact that, as the cytoplasmic buffers become saturated, a given increase in systolic total [Ca2+] produces a larger increase in free [Ca2+] and thence of Ca2+ efflux. 5. These results confirm that modulation of the ryanodine receptor has no maintained effect on systolic Ca2+ and show the interdependence of SR Ca2+ content, cytoplasmic Ca2+ buffering and sarcolemmal Ca2+ fluxes. Such analysis is important for understanding the cellular basis of inotropic interventions in cardiac muscle.
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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.