ArticleBiophysical journal2008
Effect of metabolic inhibition on couplon behavior in rabbit ventricular myocytes.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- The NADPH oxidase inhibitor diphenyleneiodonium suppresses CaThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Distinct features of calcium handling and β-adrenergic sensitivity in heart failure with preserved versus reduced ejection fraction.The Journal of physiology · 2020Article
- Metabolic Inhibition Induces Transient Increase of L-type CaInternational journal of molecular sciences · 2019Article
- Metabolic inhibition reduces cardiac L-type Ca2+ channel current due to acidification caused by ATP hydrolysis.PloS one · 2017Article
- Arrhythmogenic and metabolic remodelling of failing human heart.The Journal of physiology · 2016Review
- Regulation of calcium clock-mediated pacemaking by inositol-1,4,5-trisphosphate receptors in mouse sinoatrial nodal cells.The Journal of physiology · 2015Article
- Cardiac sodium-calcium exchange and efficient excitation-contraction coupling: implications for heart disease.Advances in experimental medicine and biology · 2013Review
- Metabolic stress, reactive oxygen species, and arrhythmia.Journal of molecular and cellular cardiology · 2012Review
- Junctophilin-2 expression silencing causes cardiocyte hypertrophy and abnormal intracellular calcium-handling.Circulation. Heart failure · 2011Article
- The Driving Force of the Na/Ca-Exchanger during Metabolic Inhibition.Frontiers in physiology · 2011Article
- Sodium-calcium exchange is essential for effective triggering of calcium release in mouse heart.Biophysical journal · 2010Article
- Role of inotropic agents in the treatment of heart failure.Circulation · 2010Article
- Cardiac metabolism and arrhythmias.Circulation. Arrhythmia and electrophysiology · 2009Review
- Loss of intracellular and intercellular synchrony of calcium release in systolic heart failure.Circulation. Heart failure · 2009Article
- New insights into the structure and function of couplons.The Journal of physiology · 2008Article
- Local calcium release activation by DHPR calcium channel openings in rat cardiac myocytes.The Journal of physiology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
We investigated the effect of combined inhibition of oxidative and glycolytic metabolism on L-type Ca(2+) channels (LCCs) and Ca(2+) spikes in isolated patch-clamped rabbit ventricular myocytes. Metabolic inhibition (MI) reduced LCC open probability, increased null probability, increased first latency, and decreased open time but left conductance unchanged. These results explain the reduction in macroscopic Ca(2+) current observed during MI. MI also produced a gradual reduction in action potential duration at 90% repolarization (APD(90)), a clear decline in spike probability, and an increase in spike latency and variance. These effects are consistent with the changes we observed in LCC activity. MI had no effect on the amplitude or time to peak of Ca(2+) spikes until APD(90) reached 10% of control, suggesting preserved sarcoplasmic reticulum Ca(2+) stores and ryanodine receptor (RyR) conductance in those couplons that remained functioning. Ca(2+) spikes disappeared completely when APD(90) reached <2% of control, although in two cells, spikes were reactivated in a highly synchronized fashion by very short action potentials. This reactivation is probably due to the increased driving force for Ca(2+) entry through a reduced number of LCCs that remain open during early repolarization. The enlarged single channel flux produced by rapid repolarization is apparently sufficient to trigger RyRs whose Ca(2+) sensitivity is likely reduced by MI. We suggest that loss of coupling fidelity during MI is explained by loss of LCC activity (possibly mediated by Ca(2+)-calmodulin kinase II activity). In addition, the results are consistent with loss of RyR activity, which can be mitigated under conditions likely to enlarge the trigger.
Indexed as
Identifiers
What OpenQuestion holds
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.