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. 2020 Mar 26;126(7):889–906. doi: 10.1161/CIRCRESAHA.119.315641

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© 2020 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 7. — I_Kur maintains brief action potential (AP) configuration in untubulated atrial myocytes, promoting early afterdepolarization (EADs) driven by nonequilibrium I_Na during hypokalemia. A, In tubulated atrial myocytes, hypokalemia-induced EADs were frequently associated with Ca²⁺ waves. B, Buffering of intracellular Ca²⁺ with patch pipettes containing 60 µmol/L EGTA reduced EAD incidence in tubulated cells. However, in untubulated cells, EADs remained present and were observed to be triggered during rapid AP repolarization from negative potentials (arrow). C, Incidence of EADs in tubulated and untubulated atrial myocytes (−EGTA: n_cells=10, 14 from 7, 8 hearts; +EGTA: n_cells=10, 11 from 6, 9 hearts). D, AP configuration in tubulated and untubulated atrial cells (n_cells=21, 48 from 12, 20 hearts). E, EADs observed in hypokalemic, untubulated atrial myocytes were inhibited by rapid application of 1 µmol/L TTX (top) or 10 mmol/L caffeine (bottom). F, Short AP configuration in untubulated atrial myocytes was associated with larger outward steady-state K⁺ current than in tubulated cells (protocol described in Online Figure IIA; n_cells=11, 22 in tubulated, untubulated from 6, 11 hearts). G, Top: steady-state current remained larger in untubulated cells after inhibition of I_TO (1 s prepulse to +50 mV, see Online Figure III; n_cells=9, 9 in tubulated, untubulated from 5, 6 hearts), but not following addition of 50 µmol/L 4-AP to inhibit I_Kur (bottom, K_o=5.0: n_cells=6, 8 from 5, 4 hearts; K_o=2.7: n_cells=6, 6 from 4, 3 hearts). H, I_Kur inhibition prolonged APD₇₅ in untubulated atrial cells during hypokalemia (n_cells=7 from 3 hearts). I, Inclusion of AP waveforms in a mathematical model of the human atrial cardiomyocyte linked EADs triggered during Ca²⁺ quiescence to reactivation of nonequilibrium I_Na, parallel involvement of a small, forward-mode NCX current (I_NCX), and subsequent recruitment of L-type Ca²⁺ current. Statistics: (C): z-test; (D, F, G, H): 2-way ANOVA with Bonferroni correction. D, Difference in means: P=1.19×10⁻³ for tubulated vs untubulated, P=1.77×10⁻⁷ for K_o=5.0 vs K_o=2.7. H, Difference in means: P=0.114. Full results of (F) and (G) are presented in Online Tables IV and V. *P<0.05 vs untubulated and †P<0.05 vs K_o=5.0.