ArticlePloS one2013
Ca²+/calmodulin-dependent protein kinase II (CaMKII) activity and sinoatrial nodal pacemaker cell energetics.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular pathways for learning in the single-cell Stentor coeruleus.Current biology : CB · 2026Article
- Aging and sinus node dysfunction: mechanisms and future directions.Clinical science (London, England : 1979) · 2025Review
- Compartmentalized cAMP signalling and control of cardiac rhythm.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2023Review
- Article
- Inhibition of adenylyl cyclase 1 by ST034307 inhibits IPFrontiers in pharmacology · 2022Article
- May the Force Not Be With You During Culture: Eliminating Mechano-Associated Feedback During Culture Preserves Cultured Atrial and Pacemaker Cell Functions.Frontiers in physiology · 2020Review
- Eliminating contraction during culture maintains global and local CaCell calcium · 2019Article
- Heart failure modulates electropharmacological characteristics of sinoatrial nodes.Experimental and therapeutic medicine · 2017Article
- Ca(2+)/calmodulin-activated phosphodiesterase 1A is highly expressed in rabbit cardiac sinoatrial nodal cells and regulates pacemaker function.Journal of molecular and cellular cardiology · 2016Article
- CaMKII-dependent phosphorylation regulates basal cardiac pacemaker function via modulation of local Ca2+ releases.American journal of physiology. Heart and circulatory physiology · 2016Article
- The Autonomic Nervous System Regulates the Heart Rate through cAMP-PKA Dependent and Independent Coupled-Clock Pacemaker Cell Mechanisms.Frontiers in physiology · 2016Article
- The end effector of circadian heart rate variation: the sinoatrial node pacemaker cell.BMB reports · 2015Review
- Real-time relationship between PKA biochemical signal network dynamics and increased action potential firing rate in heart pacemaker cells: Kinetics of PKA activation in heart pacemaker cells.Journal of molecular and cellular cardiology · 2015Article
- A Pre-clinical Animal Model of Trypanosoma brucei Infection Demonstrating Cardiac Dysfunction.PLoS neglected tropical diseases · 2015Article
- Ca2+/calmodulin potentiates I Ks in sinoatrial node cells by activating Ca2+/calmodulin-dependent protein kinase II.Pflugers Archiv : European journal of physiology · 2015Article
- Potential effects of intrinsic heart pacemaker cell mechanisms on dysrhythmic cardiac action potential firing.Frontiers in physiology · 2015Article
- From two competing oscillators to one coupled-clock pacemaker cell system.Frontiers in physiology · 2015Review
- Numerical Modeling Calcium and CaMKII Effects in the SA Node.Frontiers in pharmacology · 2014Review
- CaMKII in sinoatrial node physiology and dysfunction.Frontiers in pharmacology · 2014Review
- CaMKII inhibitors: from research tools to therapeutic agents.Frontiers in pharmacology · 2014Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelled: Ca(2+)-activated basal adenylate cyclase (AC) in rabbit sinoatrial node cells (SANC) guarantees, via basal cAMP/PKA-calmodulin/CaMKII-dependent protein phosphorylation, the occurrence of rhythmic, sarcoplasmic-reticulum generated, sub-membrane Ca(2+) releases that prompt rhythmic, spontaneous action potentials (APs). This high-throughput signaling consumes ATP.
aimsWe have previously demonstrated that basal AC-cAMP/PKA signaling directly, and Ca(2+) indirectly, regulate mitochondrial ATP production. While, clearly, Ca(2+)-calmodulin-CaMKII activity regulates ATP consumption, whether it has a role in the control of ATP production is unknown. METHODS AND
resultsWe superfused single, isolated rabbit SANC at 37°C with physiological saline containing CaMKII inhibitors, (KN-93 or autocamtide-2 Related Inhibitory Peptide (AIP)), or a calmodulin inhibitor (W-7) and measured cytosolic Ca(2+), flavoprotein fluorescence and spontaneous AP firing rate. We measured cAMP, ATP and O2 consumption in cell suspensions. Graded reductions in basal CaMKII activity by KN-93 (0.5-3 µmol/L) or AIP (2-10 µmol/L) markedly slow the kinetics of intracellular Ca(2+) cycling, decrease the spontaneous AP firing rate, decrease cAMP, and reduce O2 consumption and flavoprotein fluorescence. In this context of graded reductions in ATP demand, however, ATP also becomes depleted, indicating reduced ATP production.
conclusionsCaMKII signaling, a crucial element of normal automaticity in rabbit SANC, is also involved in SANC bioenergetics.
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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.