Aneurally cultured human muscle possesses functional dihydropyridine-sensitive voltage-dependent Ca2+ channels that mediate calcium uptake upon depolarization.
Functional DHP-sensitive Ca2+ channels mediate uptake in muscle models; leaves open clinical translation or therapeutic relevance.
Dihydropyridine-sensitive Ca2+ channels and the relationship between binding of dihydropyridine derivatives and depolarization-induced Ca2+ uptake have been studied in aneurally cultured human muscle. Analysis of the equilibrium binding of the 1,4-dihydropyridine derivative (+)-PN200-110 revealed a single high-affinity binding site with a Kd of 0.15 +/- 0.05 nM and a Bmax of 87 +/- 12 fmol/mg protein. Inhibition of (+)-[3H]PN200-110 binding by nitrendipine revealed a Ki of 0.8 nM for the nitrendipine-receptor complex. Depolarization of cultured human muscle achieved by elevating the K+ concentration increased the uptake 45Ca2+ which was inhibited by nitrendipine with an IC50 of 1.1 nM. This study demonstrates that aneurally cultured human muscle has dihydropyridine-sensitive voltage-dependent Ca2+ channels which are functional when the fibers are depolarized.
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Desnuelle et al. (1988) studied this question.
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