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. Author manuscript; available in PMC: 2006 Jun 23.
Published in final edited form as: J Cardiovasc Electrophysiol. 2006 May;17(Suppl 1):S169–S177. doi: 10.1111/j.1540-8167.2006.00401.x

Figure 6.

Figure 6

Concentration-dependent effect of ranolazine (RAN) on steady-state inactivation (SSI) of peak transient INa (INaT) and late INa (INaL) recorded in left ventricular myocytes isolated from canine failing hearts. Panel A: SSI-voltage relationship for peak INa in controls (•), and in the presence of 20 μM of ranolazine (▴), which failed to shift the SSI curve. Solid lines in Panels A and B represent data point fit to the Boltzmann function (Equation 2, Methods). All data were obtained in the same cell. Panel B: SSI-voltage relationship for late INa in controls (•) and in the presence of 5 (▪), and 10 μM ranolazine (▴), showing the leftward shift of the SSI mid-potential caused by ranolazine. All data were obtained in the same cell. Panel C: SSI mid potential shift (ΔV½) caused by ranolazine in 11 ventricular myocytes from 5 failing hearts. Solid line represents a data fit to equation 3 (Methods) to obtain dissociation constants of ranolazine for the resting (Kdr) and inactivated (Kdi) states of INaL as shown in the graph. The slope factor k in equation 3 was taken as 7.6mV, the evaluated mean for the cells presented in the panel C. Data are means ± SEM.