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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。
In order to investigate the mechanism of blood pressure-lowering in rat vascular smooth muscle cells induced by sulfur dioxide (SO2), acute smooth muscle cells of rat were isolated by acute enzyme separation method and outward potassium current (IKv) of smooth muscle cells was recorded by whole-cell patch clamp technique. SO2 and its derivatives The effect of SO2 on the potassium current in smooth muscle cells was investigated from the ion channel perspective. The results showed that the SO2 derivatives increased the IKv significantly, and the 10μmol / L SO2 derivatives significantly increased the current-voltage curve (IV curve), ie increased IKv with a certain voltage dependence. Moreover, SO2 Derivatives can increase the IKv showed a dose-response relationship. When IKv was inhibited by 5 mmol / L 4-aminopyridine (4-AP), IKv increased to a certain extent by adding 10μmol / L SO2 derivative. TEA inhibits the effect of increasing SO2 derivatives on IKv. 10μmol / L SO2 derivatives can make IKv activation curve significantly hyperpolarized shift, but does not affect the slope factor. SO2 derivatives on vascular smooth muscle cells, can cause outward potassium current amplitude increases, so that potassium current activation, which is one of the mechanism of SO2 and its derivatives antihypertensive effect; TEA, 4-AP SO2 derivatives cause Of the vascular smooth muscle cells increased potassium current antagonistic effect.