Voltage-gated sodium channel (alpha subunit) (NaV (Nav))

Voltage-gated sodium channels (NaV) are transmembrane proteins that enable the rapid influx of sodium ions during the action potential in excitable cells such as neurons and cardiac myocytes. Local anesthetics bind primarily to the intracellular portion of these channels, preferentially interacting with the open or inactivated state of the channel, stabilizing its inactive conformation. This prevents the initiation and propagation of action potentials, resulting in temporary loss of sensation or pain in the area supplied by the blocked nerve[1][2][3][4][6][9]. Local anesthetics are structurally characterized by a lipophilic aromatic ring and a hydrophilic amine, linked by either an ester or amide group. The molecules must enter the nerve cell in their unionized form to access the binding site, which is more accessible when the sodium channel is open, explaining the use- or frequency-dependence of the block[1][2][9].

Other names

Sodium channelvoltage-gated sodium channelNaV channelSCN family

Blockade of voltage-gated sodium channels in their open or inactivated state, inhibiting action potential propagation and nerve signal transmission[1][2][3][4][6][7][9][10].