Voltage-gated sodium channel and Voltage-gated calcium channel (Nav (for sodium channel), Cav (for calcium channel))

Voltage-gated sodium channels and voltage-gated calcium channels are families of closely related transmembrane ion channels that mediate the influx of sodium or calcium ions, respectively, in response to changes in membrane potential. Sodium channels are essential for the rapid rising phase of action potentials in neurons and muscle cells, playing a critical role in electrical signaling, while calcium channels translate electrical depolarization into diverse intracellular processes including neurotransmitter/hormone release, muscle contraction, and gene expression. Both are multi-subunit complexes with conserved core pore-forming alpha subunits, share similar overall topology, and are major targets for a wide range of neurological, cardiovascular, and pain therapies. Genetic or acquired dysfunction in these channels causes a spectrum of diseases termed channelopathies. Drugs that modulate these channels are widely used as local anesthetics, antiarrhythmics, anticonvulsants, and antihypertensives[5][6][7][8][3][1][2][4].

Other names

Voltage-gated sodium channelVoltage-dependent sodium channelNavNaVSCN (gene family)Voltage-gated calcium channelVoltage-dependent calcium channelCavCaVVDCC

Block of voltage-dependent opening (stabilizing the inactivated or closed state) to prevent sodium or calcium influx Use-dependent inhibition (greater block during repetitive firing) Allosteric modulation of channel gating or inactivation Alteration of channel trafficking or expression