摘要
为了探讨二氧化硫(SO2)引起大鼠血管平滑肌的降压机制,采用急性酶分离法分离大鼠单个血管平滑肌细胞,运用全细胞膜片钳技术记录平滑肌细胞外向钾电流(IKv),观察SO2及其衍生物对平滑肌细胞膜钾电流的作用,从离子通道角度研究SO2对血压的影响。结果发现:SO2衍生物可使外向IKv显著增大,10μmol/L SO2衍生物可使电流-电压曲线(I-V曲线)显著上移,即增大IKv,且呈一定的电压依赖性,并且,SO2衍生物可使IKv增大呈现出剂量-效应关系。当使用5 mmol/L 4-氨基吡啶(4-AP)抑制IKv后,加入10μmol/L SO2衍生物,IKv有一定程度增加。TEA能抑制SO2衍生物对IKv的增大效应。10μmol/L SO2衍生物可使IKv的激活曲线显著向超极化方向移动,但并不影响其斜率因子。说明SO2衍生物作用于血管平滑肌细胞,可引起外向钾电流幅度增大,使钾电流提前激活,这是SO2及其衍生物降压的作用机制之一;TEA、4-AP对SO2衍生物引起的血管平滑肌细胞钾电流的增大具有拮抗作用。
To investigate the depressing blood pressure mechanism of the sulfur dioxide（SO2） in vascular smooth muscle cells,we studied the outward potassium current（I Kv） with whole-cell configuration patch clamp technique in these cells which were obtained through acute enzyme separation method.The results show as follows：SO2 derivatives significantly increased outward I Kv which was in voltage-dependent and dose-dependent manner.10 μmol/L SO2 derivative made I-V curves significantly upward.10 μmol/L SO2 derivatives evaluated I Kv which inhabited by 5 mmol/L 4-AP.TEA inhibits which SO2 derivatives induced the augmentation of I Kv.Moreover,the sulfur dioxide derivatives at 10 μmol/L caused the activation curve to hyperpolarization without changing the slope coefficient.In conclusion,SO2 derivatives increased outward I Kv in vascular smooth muscle cells which advanced the activation of potassium current.This may be one of the mechanisms of decompression by the endogenous sulfur dioxide.TEA and 4-AP antagonized the augmentation of outward potassium current which was induced by SO2 derivatives.
出处
《生物物理学报》
CAS
CSCD
北大核心
2011年第3期203-210,共8页
Acta Biophysica Sinica
基金
山西省高校科技研发项目(200713010)
山西省大学生创新实验项目
关键词
二氧化硫
钾离子通道
膜片钳技术
血管平滑肌细胞
Sulfur dioxide
Potassium channel
Patch clamp technique
Vascular smooth muscle cells
