ArticleThe Journal of physiology2005
Different intracellular polyamine concentrations underlie the difference in the inward rectifier K(+) currents in atria and ventricles of the guinea-pig heart.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- ATP13A2 is involved in intracellular polyamine transport in lung epithelial cells.FEBS open bio · 2026Article
- A programmable ribozyme for RNA signal transduction.Nature communications · 2026Article
- The Kir2.1E299V mutation increases atrial fibrillation vulnerability while protecting the ventricles against arrhythmias in a mouse model of short QT syndrome type 3.Cardiovascular research · 2024Article
- Role of the histone tails in histone octamer transfer.Nucleic acids research · 2023Article
- ATP13A2-mediated endo-lysosomal polyamine export counters mitochondrial oxidative stress.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Ion currents, action potentials, and noradrenergic responses in rat pulmonary vein and left atrial cardiomyocytes.Physiological reports · 2020Article
- Arginase II Contributes to the CaJournal of the American Heart Association · 2018Article
- Bioelectrical control of positional information in development and regeneration: A review of conceptual and computational advances.Progress in biophysics and molecular biology · 2018Review
- External KThe Journal of general physiology · 2018Article
- Bioelectric gene and reaction networks: computational modelling of genetic, biochemical and bioelectrical dynamics in pattern regulation.Journal of the Royal Society, Interface · 2017Article
- Inter-individual variability and modeling of electrical activity: a possible new approach to explore cardiac safety?Scientific reports · 2016Article
- The inward rectifier potassium channel Kir2.1 is expressed in mouse neutrophils from bone marrow and liver.American journal of physiology. Cell physiology · 2015Article
- Inhibition of a TREK-like K+ channel current by noradrenaline requires both β1- and β2-adrenoceptors in rat atrial myocytes.Cardiovascular research · 2014Article
- Ionic mechanisms limiting cardiac repolarization reserve in humans compared to dogs.The Journal of physiology · 2013Article
- Postnatal developmental decline in IK1 in mouse ventricular myocytes isolated by the Langendorff perfusion method: comparison with the chunk method.Pflugers Archiv : European journal of physiology · 2012Article
- Experimental Mapping of the Canine KCNJ2 and KCNJ12 Gene Structures and Functional Analysis of the Canine K(IR)2.2 ion Channel.Frontiers in physiology · 2012Article
- Article
- Cardiac strong inward rectifier potassium channels.Journal of molecular and cellular cardiology · 2010Review
- Involvement of the ornithine decarboxylase/polyamine system in precondition-induced cardioprotection through an interaction with PKC in rat hearts.Molecular and cellular biochemistry · 2009Article
- Mammalian polyamine metabolism and function.IUBMB life · 2009Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The outward component of the strong inward rectifier potassium current, I(K1), is significantly larger in ventricles than in atria of the heart, resulting in faster repolarization at the final phase of the action potential in ventricles. However, the underlying mechanism of the difference in I(K1) remains poorly understood. I(K1) channels are composed of subunits from the Kir2 subfamily, and I(K1) amplitude is determined by the voltage-dependent blockade of the channel by the intracellular polyamines spermine and spermidine, and by Mg(2+). Using a perforated patch-clamp method, which minimizes changes in the intracellular polyamine and Mg(2+) concentrations, we detected repolarization-induced outward I(K1) transients, which are caused by competition between Mg(2+) and spermine to block the channel, in ventricular but not in atrial myocytes from guinea-pig heart. The contribution of the Kir2.3 subunit to the I(K1) channel was found to be minor in the guinea-pig heart, because the activation time course of the Kir2.3 currents was approximately 10-fold slower than those of I(K1), and the marked external pH sensitivity of the Kir2.3 currents was not found in I(K1). Both the Kir2.1 and Kir2.2 currents recorded from inside-out patches exhibited outward transients similar to those of ventricular I(K1) in the presence of 5-10 microM spermine and 0.6-1.1 mM Mg(2+), and their amplitudes were diminished by increasing the spermine or spermidine concentrations. The total and free polyamine concentrations in guinea-pig cardiac tissues were higher in atria than ventricles. These results strongly suggest that different intracellular polyamine concentrations are responsible for the difference in atrial and ventricular I(K1) of the guinea-pig heart.
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