摘要
目的和方法：观察虎杖甙（ＰＤ）对人脐带动脉平滑肌细胞（ＶＳＭＣ）内游离钙、细胞膜电位的变化，以探讨ＰＤ对血管平滑肌的调节机制。用Ｆｌｕｏ－３－ＡＭ、ＤｉＢＡＣ４（３）标记培养的ＶＳＭＣ，在激光共聚焦显微镜上测定细胞内游离钙和膜电位变化。结果：给ＰＤ（０５ｍｍｏｌ／Ｌ）１０ｍｉｎ后，ＶＳＭＣ内游离钙浓度升高５６％±５６％。当ＰＤ加入前用维拉帕米和ＥＧＴＡ预处理后，则游离钙不再升高；ＥＧＴＡ和肝素预处理也抑制ＰＤ的升钙作用，而ＥＧＴＡ和普鲁卡因预处理则使细胞内钙显著升高。ＰＤ还可使ＶＳＭＣ膜电位去极化，加入钠通道阻断剂河豚毒素（２５μｍｏｌ／Ｌ）可完全阻断ＰＤ的去极化作用：加甲氰咪胍、维拉帕米、优降糖和利及丁预处理不能阻断ＰＤ去极化作用。结论：：ＰＤ可通过细胞外钙内流来增加细胞内游离钙浓度。
AIM:The present study was to investigate the regulation mechanism of Polydatin on human blood vessels.METHOD:The changes of the cytosolic free calcium concentration and cell membrane potential of cultured vascular smooth muscle cells (VSMC) were determined kinetically between passages 3 and 8 isolated from human umbilicus artery.RESULTS:Polydatin (0.5 mmol/L) caused a persistent increase of intracellular calcium concentration [Ca 2+ ]i,which was inhibited completely by pretreatment with EGTA(2 mmol/L) and verapamil(50 μmol/L)10 min prior to Polydatin givening,and was also blocked completely by pretreatment with EGTA and heparin(765×10 3 U/L).But the effect of polydatin on [Ca 2+ ]i was enhanced by pretreatment with EGTA and procaine(10 mmol/L).Polydatin can also make the cell membrane potential less negative or depolarized 10 min after polydatin adding.The effects of Polydatin were enhanced significantly by pretreatment with cimetidine,but it was inhibited completely by pretreatment with tetrodotoxin(2.5μmol/L),a kind of sodium channel blocker CONCLUSIONS:Polydatin-induced alternation in[Ca 2+ ]i might be mainly due to the entry of extracellular Ca 2+ into cells and release from IP3 sensitive intracellular calcium store,and ryanodine receptor system might regulate negatively IP3 receptor system. And polydatin might induce the entry of sodium ion into cells and cause the depolarization of VSMC.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第3期233-236,共4页
Chinese Journal of Pathophysiology
关键词
血管
钙
膜电位
平滑肌细胞
虎杖甙
Muscle,smooth,vessels
Calcium
Membrane potentials
