骨格筋および心筋におけるジヒドロピリジン受容体(DHPR)以外のCa²⁺ 流入経路

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The major Ca²⁺ influx pathways through the cytoplasmic membrane in cardiac and skeletal muscles are believed to be dihydropyridine receptors (DHPR). However, we recently showed the presence of store-operated Ca²⁺ influx (SOC) pathway in skeletal muscle (Kurebayashi & Ogawa, J Physiol;2001;533;185). In this study, we intend to further characterize the properties of the SOC channel in mouse skeletal muscle and extend the study to rat cardiac muscle. In skeletal muscle, Ca²⁺ influx through the SOC channel was inward rectifying and the magnitude at the resting membrane potential was greater than that through the DHPR upon depolarization. Although severe store depletion was necessary for enhancement of Mn²⁺ influx, the Ca²⁺ entry through SOC was observed at a lesser extent of Ca²⁺ depletion, suggesting its important role in Ca²⁺ homeostasis. Among putative inhibitors of SOC, 2-aminoethoxydiphenyl borate (2-APB) was most effective. With cardiac muscle, nifedipine-insensitive Ca²⁺ entry also was detected at the resting state when the Ca²⁺ store was partially decreased. Its influx rate was lower than that through DHPR. Econazole, a putative inhibitor to TRPV5, moderately inhibited the influx whereas 2-APB did not, indicating that the Ca²⁺ influx pathway in cardiac muscle is pharmacologically different from that in skeletal muscle. Based on the above results and RT-PCR studies, candidates for these pathways will be discussed. [Jpn J Physiol 54 Suppl:S47 (2004)]