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尼可地尔降低血管平滑肌细胞内ATP诱导的游离钙浓度 |
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彭 健 何建新 刘伊丽 肖中举
摘 要 目的：探讨尼可地尔对血管平滑肌细胞内游离钙(［Ca2+］i)的影响及机理。方法：培养的兔主动脉平滑肌细胞加入Fura-2AM 2.5 μmol/L，在37℃下孵育50 min，［Ca2+］i用荧光分光光度计检测。结果：ATP(0.1 mmol/L)诱导的［Ca2+］i峰相和持续相增加可被尼可地尔抑制，且呈剂量依赖性，尼可地尔(10 μmol/L)的抑制作用可被优降糖(10 μmol/L)完全阻断(峰相：530±31 vs 544±41 nmol/L，持续相：370±19 vs 381±11 nmol/L，P＞0.05)；在无钙溶液中，先给尼可地尔能显著抑制ATP诱导的［Ca2+］i峰相增加。结论：尼可地尔抑制ATP诱导的［Ca2+］i增加，可能与减少细胞外钙内流及细胞内钙释放有关。
主题词 尼可地尔； ATP； 血管平滑肌；钙；优降糖
Nicorandil inhibits ATP-induced cytosolic free calcium increase
in cultured vascular smooth muscle cells
PENG Jian, HE Jian-Xin, XIAO Zhong-Ju1, LIU Yi-Li
Department of Internal Medicine Cardiology Division of Nanfang Hospital ;1 Department of Physiology;
The First Military Medical University, Guangzhou 510515)
Abstract AIM:To study the effects of nicorandil on cytosolic free calcium(［Ca2+］i) changes and their possible mechanisms in vascular smooth muscle cells.METHODS：Cultured rabbit aortic smooth muscle cells were treated with Fura-2 AM 2.5 μmol.L-1 at 37℃ for 50 min.［Ca2+］i level was measured by fluorospectrometer.RESULTS：ATP (0.1 mmol.L-1)-induced peak and sustained phase ［Ca2+］i increase were inhibited by nicorandil in a concentration-dependent manner. The effects of nicorandil(10 μmol.L-1) was completely canceled (peak phase:530±31 vs 544±41 nmol.L-1; sustained phase: 370±19 vs 381±11 nmol.L-1) by glibenclamide (10 μmol.L-1). Pretreated with the nicorandil, the peak ［Ca2+］i elevation induced by ATP was reduced in the Ca2+-free solution (140±22 vs 260±33 nmol.L-1,P＜0.01).CONCLUSION：Nicorandil inhibits ATP-induced［Ca2+］i increase, associated with the decreases of both Ca2+ release from intracellular store and Ca2+ influs from extracellular store.
MeSH Nicorandil; Adenosine triphosphate; Vascular smooth muscle; Calcium; Glibenclamide
尼可地尔有血管扩张作用，在冠状动脉通过激活钾通道，使膜电位超极化，钙内流减少，而扩张[1] [2] [3] 下一页
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