Weihan: this is related to voltage-dependency of inactivation (transition from closed resting to closed inactivation state) of Na channels. The more depolarized the resting potential is the less of voltage gated Na channels are available for activation

Dear Weihan: Yes, I agree with the comment by Victor Ilyin. For example, as the resting potential was set at the level of -40 mV, the magnitude of voltage-gated sodium current was completely inactivated in most of excitable cells. However, voltage-gated calcium current still exists.

Dear Weihan,

Sodium channels are voltage-dependent, usually at a resting membrane potential of around -60 to -70 mV, they are inactive. Their activation threshold is usually around -45 mV, and in an all - or- none fashion. Once they are activated excitable cells depolorize and fire action potentials and smooth muscle cells contract. If the cell is continuously depolarised to a resting membrane potential that is at or more depolorized than the level of sodium channel activation threshold (voltage), then the sodium channels are unable to remain at closed state-as their opening is also time-dependent (usually around a few seconds only). The activation and inactivation of sodium channels are also assisted by other calcium and potassium channels. In particular, K channels make up afterhyperpolarization (AHP) in excitable cells, and AHPs are critically important in repetitive activation (reactivation) of sodium channels. 

Best wishes,

Refik

Membrane hyperpolarization caused by increased amplitude of calcium-activated potassium channels is indeed able to remove inactivation of voltage-gated sodium current.

Dear three professrs, thank you for the detailed answers and pdf. They are much helpful☺