Overview
- Scholz, A. et al. (1998) J. Neurophysiol. 79, 1746.
- Shin, H.W. et al. (2014) J. Anesth. 28, 81.
Alomone Labs Bupivacaine hydrochloride blocks NaV1.2 channels expressed in Xenopus oocytes.A. Time course of NaV1.2 current amplitude, showing inhibition by 10 µM and 50 µM Bupivacaine hydrochloride (#B-125). Currents were elicited by a 100 ms voltage step from holding potential of -70 mV to 0 mV, applied every 10 seconds. B. Superimposed current traces from A at application of control, 10 µM and 50 µM Bupivacaine hydrochloride (as indicated).
Voltage-gated Na+ channels (NaV) are plasma membrane protein complexes which allow the passage of Na+ ions into cells following a change in the transmembrane voltage1,2.
NaV channels are primarily expressed in the central nervous system1,2.
Bupivacaine hydrochloride is a local anesthetic of the amino amide group. Drugs of this category induce their effect by binding to the intracellular area of the Na+ channel, which blocks the channel's ability to allow Na+ to enter the nerve cell, and thus preventing the cell's depolarization3,4.
Bupivacaine blocks both TTX-sensitive (NaV1.1, NaV1.2, NaV1.3, NaV1.4, NaV1.6 and NaV1.7) and TTX-resistant (NaV1.5, NaV1.8 and NaV1.9) NaV channels in DRG neurons with IC50 of 13 and 32 µM, respectively5.
It should also be noted that bupivacaine has an inhibitory effect on potassium channels6.
