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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Cardiovasc Drugs Ther. 2013 Feb;27(1):79–89. doi: 10.1007/s10557-012-6421-1

Fig. 6.

Fig. 6

Ranolazine produces a much greater rate-dependent inhibition of the maximal action potential upstroke velocity (Vmax) in atria than in ventricles. a Normalized changes in Vmax of atrial and ventricular cardiac preparations paced at a cycle length (CL) of 500 ms. b Ranolazine prolongs late repolarization in atria, but not ventricles and acceleration of rate leads to elimination of the diastolic interval, resulting in a more positive take-off potential in atrium and contributing to atrial selectivity of ranolazine. The diastolic interval remains relatively long in ventricles. * p<0.05 vs. control. † p<0.05 vs. respective values of M cell and Purkinje (n=7–21). From Burashnikov et al. [14], with permission