摘要
研究KATP通道开放剂尼可地尔 (Nic)对豚鼠心肌细胞膜和线粒体膜电位的影响 .用激光共聚焦显微镜和特异性荧光探针 ,观察不同剂量的Nic及KATP通道阻滞剂格列本脲 (Gli)引起急性分离的豚鼠心肌细胞膜电位 ,线粒体膜电位荧光值的变化 .Nic1mmol·L- 1引起细胞膜电位在 1min内迅速超极化〔膜电位荧光值减少 ( 75± 12 ) %〕 ,Gli 3μmol·L- 1可阻断其变化 ;0 .1和 1mmol·L- 1Nic可使线粒体膜电位去极化和膜电位荧光值在 1,2 ,5min分别增加( 12± 3) %和 ( 32± 8) % ,( 2 5± 6) %和 ( 39± 9) % ,( 34± 6) %和 ( 4 5± 12 ) % ;3μmol·L- 1Gli可抑制其变化 .结果说明低浓度Nic只引起线粒体膜电位去极化 ,高浓度Nic还可使细胞膜电位发生超极化 。
With digital imaging techniques of advanced laser confocal microscope, effects of K ATP channel opener nicorandil(Nic) on cardiac plasma membrane(CPM) and cardiac mitochondrial membrane(CMM) potential of guinea pig were studied. It was found that Nic 1 mmol·L -1 caused the potential of CPM more negative (hyperpolarization), fluorescence intensity(FI) decreased by (75±12)% of baseline within 1 min, but no effect at 0.1 mmol·L -1 . CMM was depolarized by 0.1 mmol·L -1 Nic〔FI increased by (12±3)%, (25±6)%, (34±6)% of baseline within 1, 2, 5 min〕, and by 1 mmol·L -1 Nic〔FI remarkably increased by (32±8)%, (39±9)%, (45±12)% of baseline〕. K ATP channel blocker glibenclamide 3 μmol·L -1 itself caused no effect on potential of CPM and CMM, but blocked the above effect on potential of CPM and CMM induced by Nic. The results suggest that K ATP channel of CMM is activated by low dose of Nic, and the high dose of Nic activate both K ATP channels of CPM and CMM.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2001年第1期23-26,共4页
Chinese Journal of Pharmacology and Toxicology
关键词
尼可地尔
心肌
线粒体
细胞膜
膜电位
nicorandil
myocardium
mitochondria
cell membrane, membrane potentials
