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Furthermore, I Na(L) inhibition prevented the formation of I ti and spontaneous afterdepolarizations induced by LCACs, thereby validating the temporal association of Na + accumulation with Na + /Ca 2+ -exchange and Ca 2+ overload in arrhythmogenesis ( 2+ accumulation evoked by LCAC superfusion is augmented in low extracellular Na + media, while overload does not occur with NCX1 inhibitors, NiCl 2 or amiloride ( Na(L) in LCAC-mediated arrhythmias, treatment with I Na(L) inhibitors lidocaine, ranolazine, or TTX prevents LV diastolic dysfunction in Langendorff rat hearts ( Na(L) is also suggested to reduce the metabolic deficit developed with LCAC treatment ( Na + /K + -ATPase Near consensus exists in the literature regarding LCAC inhibition of the sarcolemma NKA

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The variability that has been reported for the relevance of the AR NTD, DBD and LBD therein could be due to technical differences in the assays that were used, with some groups performing solely biochemical assays and recombinant AR domain(s) and others combining these with cell line studies

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