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. Author manuscript; available in PMC: 2014 Jun 7.
Published in final edited form as: Circ Res. 2013 Apr 22;112(12):1567–1576. doi: 10.1161/CIRCRESAHA.112.300370

Figure 1. β-AR enhances ICa,L in mouse ventricular cardiomyocytes via the activation of ACVI.

Figure 1

(a) Representative ICa,L recorded from ventricular myocytes isolated from WT, ACV KO, and ACVI KO, respectively. Current traces were elicited using a voltage step of 0 mV for 500 ms from a holding potential of -55 mV at baseline (blue) and after 20 minutes of ISO (red). The corresponding currentvoltage (IV) relations elicited using a family of voltage steps from -40 to +60 mV from a holding potential of -55 mV are shown to the right. (b) Schematic representation of the known regulation of ICa,L by β-AR stimulation. (c) Summary data of ICa,L density (in pA/pF) from the three groups of mice (n=8 for each group, *P<0.05).