Abstract

Editorial: Ca(2+) Signaling and Heart Rhythm.

Highlights

  • Specialty section: This article was submitted to Cardiac Electrophysiology, a section of the journal Frontiers in Physiology

  • Ca2+ is a strategic intracellular second messenger regulating multifarious cardiac cellular processes. This Frontiers issue on Ca2+ signaling and cardiac rhythm first focuses on the spontaneous membrane depolarization triggering action potential (AP) pacing by sino-atrial node (SAN) cells

  • Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels carrying If likely importantly contribute to this process: Hcn4-/- and Hcn4R669Q/R669Q mouse embryos were bradycardic with 75–90% reduced If before eventual lethality (Stieber et al, 2003; Chandra et al, 2006; Harzheim et al, 2008); tamoxiphen-inducible adult hearts showed ∼70% reduced If and progressive ≤50% reductions in, persistent, SAN pacing, compromising its responses to isoproterenol challenge (Sohal et al, 2001; Baruscotti et al, 2011)

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Summary

Introduction

Specialty section: This article was submitted to Cardiac Electrophysiology, a section of the journal Frontiers in Physiology. This Frontiers issue on Ca2+ signaling and cardiac rhythm first focuses on the spontaneous membrane depolarization triggering action potential (AP) pacing by sino-atrial node (SAN) cells. Classic pharmacological and immunological localization studies had implicated sarcoplasmic reticular (SR)-mediated Ca2+ storage and release (Rigg and Terrar, 1996) involving ryanodine receptor (RyR2)-Ca2+ release channels (Rigg et al, 2000) as necessary components in an adrenergically-responsive, complex, Ca2+-dependent, sinoatrial pacing process.

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