Add time:09/30/2019 Source:sciencedirect.com
There have been few reports on the mechanism(s) of action of oxethazaine (OXZ) despite its potent local anesthetic action. Generally, local anesthetics (LAs) not only inhibit Na+ channels but also affect various membrane functions. In the present study, using PC12 cells as a nerve cell model, the effects of OXZ on intracellular Ca2+ concentration ([Ca2+]i) were examined in relation to cytotoxicity and dopamine release. [Ca2+]i was determined by the quin2 method. In resting cells, (6–10)×10−5 M OXZ produced lactate dehydrogenase leakage, which was Ca2+-dependent, inhibited by metal Ca2+ channel blockers, and preceded by a marked increase in [Ca2+]i. Some other LAs showed no cytotoxicity at these concentrations. In K+-depolarized cells, however, lower concentrations of OXZ (10−6–10−7 M), that had no effect on resting [Ca2+]i, inhibited both the dopamine release and the increase of [Ca2+]i in parallel. The inhibitory potency against the [Ca2+]i increase was in the order of nifedipine>OXZ∼verapamil>diltiazem, and OXZ acted additively on the Ca2+ channel blockers. OXZ showed the least effect on K+-depolarization as determined by bisoxonol uptake. OXZ also inhibited the increase in [Ca2+]i induced by S(−)-BAY K 8644, a Ca2+ channel agonist. These observations suggested that low concentrations of OXZ interact with L-type Ca2+ channels. The biphasic effects of OXZ on Ca2+ movement may be due to a unique chemical structure, and may participate in and complicate the understanding of the potent pharmacological and toxicological actions of OXZ.
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