Han J, Kim E, Ho W K, Earm Y E
Department of Physiology and Biophysics, College of Medicine, Inje University, Korea.
Biochem Biophys Res Commun. 1996 Feb 27;219(3):900-3. doi: 10.1006/bbrc.1996.0330.
The properties of sulfhydryl redox modulation of the ATP-sensitive K+ K(ATP) channel have been examined in rabbit ventricular myocytes, using the patch-clamp technique. The sulfhydryl oxidizing agent 5.5'-dithio bis-(2-nitro-benzoic acid) (DTNB) induced an inhibition of the channel activity without change in the single channel conductance. DTNB had no effect on the inhibitory action by ATP. Analysis of the open and closed time distributions showed that DTNB decreased the life time of bursts and increased the interburst interval without changes in open and closed time distributions shorter than 5 ms. N-ethylmaleimide (NEM), a substance that reacts with sulfhydryl groups of cysteine residues in proteins, induced an irreversible closure of the channel. The results suggested that changes in the sulfhydryl redox also modulate K(ATP) channel activity of the K(ATP) channel in rabbit ventricular myocytes.
运用膜片钳技术，在兔心室肌细胞中研究了ATP敏感性钾通道（K(ATP)通道）的巯基氧化还原调节特性。巯基氧化剂5,5'-二硫代双（2-硝基苯甲酸）（DTNB）可抑制通道活性，但单通道电导无变化。DTNB对ATP的抑制作用无影响。对开放和关闭时间分布的分析表明，DTNB缩短了爆发持续时间，增加了爆发间期，而短于5毫秒的开放和关闭时间分布无变化。N-乙基马来酰亚胺（NEM）是一种能与蛋白质中半胱氨酸残基的巯基发生反应的物质，可使通道不可逆关闭。结果提示，巯基氧化还原变化也可调节兔心室肌细胞中K(ATP)通道的K(ATP)通道活性。
