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. Author manuscript; available in PMC: 2024 Jan 1.
Published in final edited form as: J Physiol. 2022 Dec 14;601(1):51–67. doi: 10.1113/JP283870

Fig. 7. Activation of SK channels reduces risk for CaT alternans in myocytes with simulated LQTS type-1 and type-2.

Fig. 7

A: (a) Overlay of APs recorded from the same ventricular myocyte in control and after application of Kv7.1 blocker HMR1556 (1 μM). (b) Mean and individual cell APD50, APD70 and APD90 data in control and in the presence of HMR1556 (n/N=8/4; paired t test).

B: (a) Time course of APD70 changes during application of HMR1556 alone and simultaneously with NS309. (b) Mean and individual cell APD70 data recorded in control, in the presence of HMR1556, followed by simultaneous application of NS309 and HMR1556 (n/N=6/3).

C: Mean and individual cell CaT ARs observed in field stimulated ventricular myocytes in control and after application of HMR1556 (n/N = 17/7; paired t test).

D: (a) CaT alternans observed in control and in the presence of 1 μM HMR1556, subsequently abolished by NS309 application in the presence of HMR1556.

(b) Mean and individual cell CaT ARs recorded from field stimulated ventricular myocytes in control, in the presence of HMR1556, followed by simultaneous application of HMR1556 and NS309 (n/N=7/3, Tukey’s multiple group comparison test).

E: Mean and individual cell CaT ARs observed in control, in the presence of 1 μM E4031, and during simultaneous application of E4031 and NS309 (n/N=8/3).