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Pacemaker channels and sinus node arrhythmia.

Juliane Stieber·Franz Hofmann·Andreas Ludwig
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Abstract

Cardiac pacemaker activity is regulated by at least five different classes of ion channels and by the opposing influence of sympathetic and parasympathetic stimulation. Inactivation of several genes, including a subunit coding for the potassium channel activated by the muscarinic receptor, I(KACh); the calcium channel, I(Ca,); and the hyperpolarization-activated channel, I(f), results in sinus node arrhythmia. Inactivation of the gene for the hyperpolarization-activated, cyclic nucleotide-gated channel isoform HCN2 or HCN4 and the use of pacemaker channel blockers show that (a) HCN2 prevents the diastolic membrane potential from becoming too negative, (b) HCN4 is the major channel mediating sympathetic stimulation of the pacemaker activity, and (3) complete blockage of the I(f) current is compatible with slow sinus node rhythm.

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Action PotentialsAnimalsArrhythmia, SinusCyclic Nucleotide-Gated Cation ChannelsElectrophysiologyHeart RateHumansHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsIon ChannelsMiceMice, KnockoutMuscle ProteinsPotassium ChannelsRabbitsRisk FactorsSensitivity and SpecificitySinoatrial NodeJournal ArticleResearch Support, Non-U.S. Gov'tReview

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BibTeXRIS

Juliane Stieber, Franz Hofmann, Andreas Ludwig. 2004. Pacemaker channels and sinus node arrhythmia.. https://doi.org/10.1016/j.tcm.2003.09.006

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