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Updated: May 30, 2025

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
From Atrial Small-conductance Calcium-activated Potassium Channels to New Antiarrhythmics
Arnela Saljic1,2, Jordi Heijman3,4, Dobromir Dobrev1,5,6
1Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen Copenhagen, Denmark.
Abstract:
Despite significant advances in its management, AF remains a major healthcare burden affecting millions of individuals. Rhythm control with antiarrhythmic drugs or catheter ablation has been shown to improve symptoms and outcomes in AF patients, but current treatment options have limited efficacy and/or significant side-effects. Novel mechanism-based approaches could potentially be more effective, enabling improved therapeutic strategies for managing AF. Small-conductance calcium-activated potassium (SK or KCa2.x) channels encoded by KCNN1-3 have recently gathered interest as novel antiarrhythmic targets with potential atrial-predominant effects. Here, the molecular composition of smallconductance calcium-activated potassium channels and their complex regulation in AF as the basis for understanding the distinct mechanism of action of pore-blockers (apamin, UCL1684, ICAGEN) and modulators of calcium-dependent activation (NS8593, AP14145, AP30663) are summarised. Furthermore, the preclinical and early clinical evidence for the role of small-conductance calcium-activated potassium channel inhibitors in the treatment of AF are reviewed.
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