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- W2091502023 abstract "Ranolazine is a clinically approved anti-anginal drug with potential antiarrhythmic, antiepileptic, and analgesic applications. The therapeutic effects of ranolazine are dependent on its ability to preferentially inhibit persistent currents in a variety of voltage-gated sodium channels. Extracellular acidosis, as occurs during ischemic events, may alter the interaction between ranolazine and the channel. In this study, we performed whole-cell patch clamp experiments with extracellular solution titrated to pH 7.4 or pH 6.0 using HEK cells expressing NaV1.5 and CHO cells expressing NaV1.2. We found that ranolazine modulates these sodium channels with onset/recovery kinetics and voltage-dependence resembling slow inactivation. In this way, ranolazine increases use-dependent inactivation of the channel and decreases window currents. At pH 6.0, ranolazine interaction with the sodium channel is slowed approximately 4-5 fold in both NaV1.2 and NaV1.5. Despite the slowed kinetics, ranolazine remains effective at steady-state during acidic conditions. At low extracellular pH ranolazine rescues the voltage-dependence of slow inactivation at a therapeutically relevant concentration (10µM). Our results suggest that, at pH 6.0, ranolazine compensates for proton-induced impaired slow inactivation and remains effective at reducing persistent currents." @default.
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- W2091502023 date "2013-01-01" @default.
- W2091502023 modified "2023-10-18" @default.
- W2091502023 title "Proton Modulation of Ranolazine Effects on Slow Inactivation in Sodium Channels" @default.
- W2091502023 doi "https://doi.org/10.1016/j.bpj.2012.11.763" @default.
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