摘要
目的 从离子通道水平 ,探讨前列腺素E1(PGE1)对ATP敏感K+ (KATP)通道的作用。方法 膜片钳制技术全细胞记录模式。结果 PGE1可诱导KATP通道开放并呈浓度依赖关系。保持电位 - 40mV ,指令电位 +2 0mV ,持续时间 1s条件下 ,10 μmol·L-1PGE1使外向K+ 电流由给药前的 (2 2 7± 0 34 )nA增加到 (5 46± 0 34 )nA(n =6 ,P <0 0 1) ,增加了 (3 18± 0 2 3)nA。并且增加的钾电流可被KATP通道特异阻断剂Glibenclamide(10 μmol·L-1)抑制 ,抑制率是 6 3%± 7% (n =5 ,P <0 0 1)。
AIM To investigate the effect of prostaglandin E 1(PGE 1) on ATP sensitive K + (K ATP ) channel in ventricular myocytes of guinea pig and explain the physiological , pathophysiological and pharmacological mechanism of PGE 1 on channel level. METHODS Patch clamp technique with standard whole cell configuration. Holding potential was -40 mV, commanding potential was -100 mV～+60 mV, and duration was 1 s. RESULTS PGE 1 induced K ATP channel opening in a concentration dependent manner. When holding potential was -40 mV and command potential was +20 mV, K + current increased from (2 27±0 34) nA to (5 46±0 34) nA( n=6, P <0 01) after perfusion with external solution containing 10 μmol·L -1 PGE 1. The increased K + current could inhibit by specific K ATP channel inhibitor glibenclamide (10 μmol·L -1 ), and inhibitory rate was 63%±7%( n=6,P <0 01). CONCLUSION PGE 1 opens K ATP channel in ventricular myocyte of guinea pig.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2001年第3期326-328,共3页
Chinese Pharmacological Bulletin
基金
辽宁省自然科学基金!资助项目
No 6190 73
