Tomokazu Watano (1), Hideaki Hara (2,*) and Takayuki Sukamoto (2)
(1) Department of Pharmacology, New Drug Discovery Research Laboratory
and (2) Department of Pharmacology, New Drug R & D Laboratory, Kanebo
Ltd., 1-5-90 Tomobuchi-cho, Miyakojima-ku, Osaka 534, Japan
(*) To whom correspondence should be addressed.
Abstract: We investigated the effect of lomerizine, an anti-migraine
drug, on the Ba2+ current through voltage-gated Ca2+ channels in rat pheochromocytoma
(PC12) cells using a whole-cell voltage-clamp technique. Lomerizine inhibited
the Ba2+ current with an IC50 value of 1.9 microM. Lomerizine and nicardipine
were >4 times more potent than flunarizine, diltiazem, verapamil and
dimetotiazine. The time course of inactivation induced by lomerizine was
similar to that induced by nicardipine and flunarizine. These data indicate
that lomerizine may inhibit the Ca2+ channel in a similar manner to nicardipine
and flunarizine, and its potency is almost equal to that of nicardipine.
Keywords: Lomerizine, Voltage-gated Ca2+ channel, PC12 cell