Overview
- Tagariello, V. et al. (2001) Minerva Anestesiol. 67, 5.
- Bräu, M. E. et al. (1998) Anesth. Analg. 87, 885.
- Kindler, C. H. et al. (1999) Anesthesiology 90, 1092.
Alomone Labs Mepivacaine hydrochloride blocks NaV1.7 channels expressed in Xenopus oocytes.A. Time course of NaV1.7 current amplitude, showing reversible inhibition by 175 µM Mepivacaine hydrochloride (#M-110). Currents were elicited by a 100 ms voltage step to -10 mV from a slightly depolarized holding potential of -70 mV, applied every 10 seconds. B. Superimposed current traces from A, upon application of control and of 175 µM Mepivacaine hydrochloride (as indicated).
Local anesthetics block propagation of compound action potentials by binding to voltage-gated sodium (Na+) channels1 but also potently block potassium (K+) currents2.
Mepivacaine hydrochloride has similar time of anesthesia as Lidocaine. Both anesthetics are adequate for surgical procedures that last one hour and there is no difference between them in relation to the severity of dentistry post-operative pain3,4.
Mepivacaine reversibly blocks transient Na+ inward current, as well as steady-state K+ outward current, in sciatic nerve fibers of Xenopus laevis, with half-maximal tonic inhibiting concentrations (IC50) values of 149 μM and 2305 μM, respectively5.
It blocks tandem pore domain K+ channel (TASK) with an IC50 value of 709 μM6 and the open state of hKV1.5 channel7.
