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Updated: Aug 29, 2026

Microelectrode Array Recording of Sinoatrial Node Firing Rate to Identify Intrinsic Cardiac Pacemaking Defects in Mice
Published on: July 5, 2021
Pacemaker channels and sinus node arrhythmia
Juliane Stieber1, Franz Hofmann, Andreas Ludwig
1Institut für Pharmakologie und Toxikologie, Technische Universität München, Munich, Germany.
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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