Disruption of actin cytoskeleton attenuates sulfonylurea inhibition of cardiac ATP-sensitive K+ channels.
Disruption of actin cytoskeleton attenuates sulfonylurea inhibition of cardiac ATP-sensitive K+ channels.
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肌动蛋白细胞骨架的破坏会减弱磺酰脲类对心脏 ATP 敏感 K 通道的抑制作用。
DOI：
10.1007/s004240050384
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Sperelakis,N
中科院分区：
文献类型：
--
作者：
Yokoshiki,H;Katsube,Y;Sunugawa,M;Seki,T;Sperelakis,N
两种肌动蛋白降解剂，DNA酶I和细胞松弛素D，被用来检查参与的磺酰脲受体（SUR）和ATP敏感的K+（KATP）通道之间的功能相互作用的细胞骨架。分离的大鼠心室肌细胞进行了研究，使用开放的细胞贴附单通道记录的补丁。DNA酶I（100 μg/ml）或细胞松弛素D（10 μM）刺激KATP通道活性（在30 μM ATP存在下），这些通道对甲苯磺丁脲（0.5mM）的抑制有抵抗力。暴露于甲苯磺丁脲后，在不存在肌动蛋白破坏物的对照斑中的相对NPo值为0.09 ± 0.02，在用DNA酶I或细胞松弛素D处理的细胞中分别为0.67 ± 0.22* 或0.65 ± 0.10*（*P< 0.05 vs.对照）。DNase I可减弱格列本脲（10 μM）对KATP通道的抑制作用。因此，肌动蛋白细胞骨架的破坏减弱了SUR抑制KATP通道开放的能力。
Two actin filament-depolymerizing agents, DNase I and cytochalasin D, were used to examine the involvement of the cytoskeleton in the functional interaction between the sulfonylurea receptor (SUR) and the ATP-sensitive K+(KATP) channels. Isolated rat ventricular cardiomyocytes were studied using open cell-attached patches for single-channel recording. Bath application of DNase I (100 μg/ml) or cytochalasin D (10 μM) stimulated the KATPchannel activities (in presence of 30 μM ATP), and these channels became resistant to inhibition by tolbutamide (0.5 mM). After exposure to tolbutamide, the relative NPovalue was 0.09 ± 0.02 in control patches in absence of actin disrupters, and 0.67 ± 0.22* or 0.65 ± 0.10*, respectively, in cells treated with DNase I or cytochalasine D (*P< 0.05 vs. control). The inhibitory action of glibenclamide (10 μM) on the KATPchannels was also attenuated by DNase I. Thus, the disruption of the actin cytoskeleton attenuates the ability of SUR to inhibit the opening of KATPchannels.