Michiaki Yamakage1, Akiyoshi Namiki. 1. Department of Anesthesiology Sapporo Medical University School of Medicine Sapporo Hokkaido Japan. yamakage@sapmed.ac.jp
Abstract
PURPOSE: To 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. SOURCE: The information was obtained from articles published recently and from our published work. PRINCIPAL FINDINGS: Voltage-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. CONCLUSION: Recent 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.
PURPOSE: To 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. SOURCE: The information was obtained from articles published recently and from our published work. PRINCIPAL FINDINGS: Voltage-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. CONCLUSION: Recent 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.
Authors: Ruma Mukerjee; J Robert Chang; Luis Del Valle; Asen Bagashev; Monika M Gayed; Randolph B Lyde; Brian J Hawkins; Eugen Brailoiu; Eric Cohen; Chris Power; S Ausim Azizi; Benjamin B Gelman; Bassel E Sawaya Journal: J Biol Chem Date: 2011-08-04 Impact factor: 5.157