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. Author manuscript; available in PMC: 2021 Nov 17.
Published in final edited form as: Circulation. 2020 Sep 15;142(20):1937–1955. doi: 10.1161/CIRCULATIONAHA.120.046450

Figure 6. β-adrenergic receptor stimulation enhances peak and late ICa.L during the action potential in Calm1N98S/+ ventricular myocytes.

Figure 6.

A and B, L-type Ca2+ currents (lower panels) elicited by “typical” action potential waveforms (upper panels) that had been pre-recorded from isoproterenol (50 nM) - treated Calm1+/+ and Calm1N98S/+ ventricular myocytes. Action potential waveforms were delivered at 1 Hz steady-state frequency in the presence of isoproterenol (50 nM). Each data point in an ICa.L trace represents the mean ± SEM of 20 and 22 cells isolated from 4 Calm1+/+ and 4 Calm1N98S/+ hearts, respectively. C and D, The same action potential waveforms and ICa.L traces shown in A and B at expanded time scales. E and F, Dot plots of total ICa.L (∫ICa.L; E) normalized to cell capacitance and peak ICa.L density during the ventricular action potential in isoproterenol-treated cardiomyocytes. AP: action potential. Horizontal lines indicate mean ± SEM; 20 cells from 4 Calm1+/+ mice and 22 cells from 4 Calm1N98S/+ mice. P values by ANOVA followed by Bonferroni test for post hoc comparison.