We reviewed recent works on molecular biological and electrophysiological and kinetic studies on Na channels in the first part of the paper. Special emphasis was laid on Kuo-Bean model, on which our simulation study in the second part was based. We also stated the process through which this model was presented as a development of the classical Hodgkin-Huxley theory. In the second part, we discussed on presumptive four bindings sites for lidocaine (Lid) and related class I antiarrhythmic and local anesthetic drugs in the Na channels. The first is within the ion conduction pore, related to open channel blocking actions, and the action on this site may be particularly conspicuous in the nerve Na channel isomers. This second is the site that is related to the stabilization of the inactivated state and relevant to the action of antiarrhythmic drugs of an inactivation channel blocking type. Modeling of kinetics of Lid is attempted here on the extension of Kuo-Bean model. The third is the site relevant to the block of slow inactivation. We have little information on this site. The fourth is the site surmised from gating current studies by Sheets and Hanck and binding of a drug to this site is supposed to restrict the movement of voltage sensor, S4. In considering the intimate relation between voltage-sensor, activation, deactivation and inactivation, drastic movement of S4, and pharmacological differences between nerve, skeletal muscle and heart Na channel isomers, we discussed a possibility of formation of a new site by fusion of the second and fourth sites and annular lipid surrounding the channel.