Overview
- Watano, T. et al. (1997) Jpn. J. Pharmacol. 75, 209.
- Iwamoto, T. et al. (1988) Jpn J Pharmacol 48, 241.
Alomone Labs Lomerizine dihydrochloride inhibits L-type voltage-gated CaV1.2 currents heterologously expressed in Xenopus oocytes.A. Time course of CaV1.2/α2-δ1/β2a (L-type) current inhibition by 10 and 100 µM Lomerizine dihydrochloride (#L-125). Currents were elicited by application of voltage steps from a holding potential of -100 mV to 0 mV (100 msec). B. Superimposed example traces of current responses before and during perfusion of 10 and 100 µM Lomerizine dihydrochloride as indicated.
Voltage-dependent L-type Ca2+ channels play an important role Ca2+ influx. L-type calcium currents typically require a strong depolarization for activation and are long-lasting1.
The common pharmacological profile of L-type channels is determined by the α1 subunit, which forms the Ca2+ selective pore, and is encoded by one of the CaV1 (α 1S) channel genes2. Cav1.2 (CACNA1C) in humans is widely expressed in cardiac myocytes, smooth muscle myocytes, endocrine cells, neuronal cell bodies and proximal dendrites1.
Lomerizine dihydrochloride is a Ca2+ channel blocker with relatively selective CNS effects. Lomerizine was developed as a potential agent for the selective improvement of the ocular or cerebrovascular circulation with minimal adverse cardiovascular effects3, and it is used as an anti migraine drug4. Lomerizine selectively relaxes smooth muscle cells by inhibiting L-type Ca2+ influx, thereby reducing tone and increasing blood flow in cerebral vessels4.
Lomerizine blocked Ba2+ current through the voltage-gated Ca2+ channel in rat pheochromocytoma (PC12) cells5, and it is suggested to bind to the 1,4-dihydropyridine binding site, as obtained by a [3H]nitrendipine binding study6.
