Articaine blocks nerve conduction by reversibly binding to the -subunit of the voltage-gated sodium channels within the inner cavity of the nerve, similar to other local anesthetics. Binding of articaine to the sodium channel reduces sodium influx so that the threshold potential will not be reached and impulse conduction stops. The blocking action of articaine on the sodium channel is state dependent: it has the highest affinity for the open state, an intermediate affinity for the inactivated state, and the lowest affinity for the resting state
The degree of neuronal block is affected by the diameter of the nerve. Larger-diameter fibers (touch/pressure/ motor) require higher concentrations of local anesthetic compared with small myelinated fibers (pain afferents). Articaine is lipid soluble, highly protein-bound (94%), and has a dissociation constant (pKa) of 7.8. Articaine is an intermediate-potency, short-acting local anesthetic with a fast onset of action