ArticleThe Journal of physiology2006
Calmodulin kinase II accelerates L-type Ca2+ current recovery from inactivation and compensates for the direct inhibitory effect of [Ca2+]i in rat ventricular myocytes.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Reduced O-GlcNAcylation diminishes cardiomyocyte CaJournal of molecular and cellular cardiology · 2023Article
- L-type CaPhysiological reports · 2022Article
- Wenxin Keli for the Treatment of Arrhythmia-Systems Pharmacology andFrontiers in pharmacology · 2021Article
- Determinants of Ca2+ release restitution: Insights from genetically altered animals and mathematical modeling.The Journal of general physiology · 2020Article
- A combined CaMKII inhibition and mineralocorticoid receptor antagonism via eplerenone inhibits functional deterioration in chronic pressure overloaded mice.Journal of cellular and molecular medicine · 2020Article
- Arrhythmogenic Mechanisms in Heart Failure: Linking β-Adrenergic Stimulation, Stretch, and Calcium.Frontiers in physiology · 2018Review
- The calcium-frequency response in the rat ventricular myocyte: an experimental and modelling study.The Journal of physiology · 2016Article
- Computational analysis of the regulation of Ca(2+) dynamics in rat ventricular myocytes.Physical biology · 2015Article
- New antiarrhythmic targets to control intracellular calcium handling.Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2014Article
- Ca(2+) current facilitation is CaMKII-dependent and has arrhythmogenic consequences.Frontiers in pharmacology · 2014Review
- Rate-dependent Ca2+ signalling underlying the force-frequency response in rat ventricular myocytes: a coupled electromechanical modeling study.Theoretical biology & medical modelling · 2013Article
- The promise of CaMKII inhibition for heart disease: preventing heart failure and arrhythmias.Expert opinion on therapeutic targets · 2013Review
- The interaction of Ca2+ with sarcomeric proteins: role in function and dysfunction of the heart.American journal of physiology. Heart and circulatory physiology · 2012Review
- Facilitation and Ca2+-dependent inactivation are modified by mutation of the Ca(v)1.2 channel IQ motif.The Journal of biological chemistry · 2011Article
- Electromechanical coupling in the cardiac myocyte; stretch-arrhythmia feedback.Pflugers Archiv : European journal of physiology · 2011Review
- Cardiac calmodulin kinase: a potential target for drug design.Current medicinal chemistry · 2011Review
- Synaptic vesicles control the time course of neurotransmitter secretion via a Ca²+/H+ antiport.The Journal of physiology · 2011Article
- Alterations of L-type calcium current and cardiac function in CaMKII{delta} knockout mice.Circulation research · 2010Article
- Cardiomyocytes with disrupted CFTR function require CaMKII and Ca(2+)-activated Cl(-) channel activity to maintain contraction rate.The Journal of physiology · 2010Article
- Facilitation of murine cardiac L-type Ca(v)1.2 channel is modulated by calmodulin kinase II-dependent phosphorylation of S1512 and S1570.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Some studies report that the positive relationship between L-type Ca(2+) current (I(Ca-L)) and frequency in cardiac myocytes is mainly due to a direct negative feedback of sarcoplasmic reticulum Ca(2+) release on I(Ca-L) inactivation while others provide evidence for activation of calmodulin kinase II (CaMKII). To further elucidate the role of endogenous CaMKII activity, the CaMKII inhibitory peptides, autocamtide-2 relating inhibitory peptide (AIP) and myristoylated AIP were applied using conventional and perforated patch-clamp methods. AIP inhibited the normal adaptive increase in I(Ca-L) in response to abrupt increase in pacing frequency from 0.05 to 2 Hz. The positive I(Ca-L)-frequency relationship was reversed by AIP and the inhibitory effect of AIP was significantly exaggerated at fast pacing rates. The onset of inactivation of I(Ca-L) was not altered by AIP. After thapsigargin treatment, AIP slowed recovery from inactivation of I(Ca-L) and this effect was exaggerated during fast pacing. Buffering of [Ca(2+)](i) by BAPTA and EGTA accelerated recovery of I(Ca-L) from inactivation, and BAPTA partly eliminated the effect of AIP on the recovery. We conclude that: (1) [Ca(2+)](i) directly slows I(Ca-L) recovery from inactivation; and (2) Ca(2+)-dependent endogenous CaMKII activity accelerates the I(Ca-L) recovery. Thus, at fast heart rates, elevated [Ca(2+)](i) activates endogenous CaMKII and compensates for its direct inhibitory effect on I(Ca-L) recovery from inactivation. Dynamic activity of endogenous CaMKII enhances the positive I(Ca-L)-frequency relationship.
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