• Michiaki Yamakage and Akiyoshi Namiki.
• Department of Anesthesiology Sapporo Medical University School of Medicine Sapporo Hokkaido Japan. yamakage@sapmed.ac.jp
• Can J Anaesth. 2002 Feb 1; 49 (2): 151-64.

PurposeTo review recent findings concerning Ca(2+) channel subtype/structure/function from electrophysiological and molecular biological studies and to explain Ca(2+) channel diseases and the actions of anesthetics on Ca(2+) channels.SourceThe information was obtained from articles published recently and from our published work.Principal FindingsVoltage-dependent Ca(2+) channels serve as one of the important mechanisms for Ca(2+) influx into the cells, enabling the regulation of intracellular concentration of free Ca(2+). Recent advances both in electrophysiology and in molecular biology have made it possible to observe channel activity directly and to investigate channel functions at molecular levels. The Ca(2+) channel can be divided into subtypes according to electrophysiological characteristics, and each subtype has its own gene. The L-type Ca(2+) channel is the target of a large number of clinically important drugs, especially dihydropyridines, and binding sites of Ca(2+) antagonists have been clarified. The effects of various kinds of anesthetics in a variety of cell types have been demonstrated, and some clinical effects of anesthetics can be explained by the effects on Ca(2+) channels. It has recently become apparent that some hereditary diseases such as hypokalemic periodic paralysis result from calcium channelopathies.ConclusionRecent advances both in electrophysiology and in molecular biology have made it possible to clarify the Ca(2+) channel structures, functions, genes, and the anesthetic actions on the channels in detail. The effects of anesthetics on the Ca(2+) channels either of patients with hereditary channelopathies or using gene mutation techniques are left to be discovered.

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