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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－２ＡＭ２５μｍｏｌ／Ｌ，在３７℃下孵育５０ｍｉｎ，［Ｃａ２＋］ｉ用荧光分光光度计检测。结果：ＡＴＰ（０１ｍｍｏｌ／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（１０μｍｏｌ／Ｌ）的抑制作用可被优降糖（１０μｍｏｌ／Ｌ）完全阻断（峰相：５３０±３１ｖｓ５４４±４１ｎｍｏｌ／Ｌ，持续相：３７０±１９ｖｓ３８１±１１ｎｍｏｌ／Ｌ，Ｐ＞００５）；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。
Objective: To investigate the effect and mechanism of nicorandil on intracellular free calcium ([Ca2 +] i) in vascular smooth muscle cells. Methods: Rabbit aortic smooth muscle cells were cultured with Fura-2AM25μmol / L and incubated at 37 ℃ for 50min. [Ca2 +] i was detected by fluorescence spectrophotometer. RESULTS: The (Ca 2+] i peak phase and the sustained phase increase induced by ATP (0.1 mmol / L) were inhibited by nicorandil in a dose-dependent manner. The inhibitory effect of nicorandil (10 μmol / L) (10μmol / L) were completely blocked (peak phase: 530 ± 31vs544 ± 41nmol / L, continuous phase: 370 ± 19vs381 ± 11nmol / L, P> 005); in the calcium-free solution, Codil significantly inhibited ATP-induced [Ca 2+] i peak phase increase. Conclusion: Nicorandil inhibits the increase of [Ca2 +] i induced by ATP, which may be related to the decrease of extracellular calcium influx and intracellular calcium release.