急性缺氧对环匹阿尼酸诱导的大鼠远端肺静脉平滑肌细胞内钙浓度升高的影响

发布时间：2018-05-30 18:43

本文选题：急性缺氧 + 环匹阿尼酸　；参考：《中国循环杂志》2015年08期

【摘要】：目的:研究急性缺氧对Ca2+-ATPase抑制剂——环匹阿尼酸(CPA)诱导的大鼠远端肺静脉平滑肌细胞(PVSMC)内钙浓度([Ca2+]i)升高的影响及机制。方法:选用6只雄性SD大鼠(体重200~250 g),培养大鼠PVSMC,运用荧光显微镜和细胞内钙浓度检测系统观测CPA及急性缺氧(4%O2)对PVSMC的[Ca2+]i影响及钙池操纵性钙通道(SOCC)阻断剂氯化镍(Ni Cl2)和SKF96365的干预作用。结果:含5μmol/L硝苯地平(电压依赖钙通道阻断剂)的无钙Krebs溶液孵育PVSMC,10μmol/L CPA使PVSMC的[Ca2+]i小幅度升高,急性缺氧能使[Ca2+]i升高幅度增加;恢复细胞外Ca2+至2.5 mmol/L后,10μmol/L CPA使[Ca2+]i显著升高,急性缺氧可导致CPA诱导的[Ca2+]i升高显著增强;SOCC阻断剂Ni Cl2(500μmol/L)和SKF96365(50μmol/L)均能明显抑制急性缺氧条件下CPA诱导的[Ca2+]i升高,但对高钾(60 mmol/L KCl)Krebs溶液引起的[Ca2+]i反应无影响。结论:急性缺氧能够使CPA诱导的大鼠远端PVSMC的[Ca2+]i升高增强,[Ca2+]i升高可被SOCC阻断剂阻断,提示急性缺氧能够增强SOCC活性,使细胞外Ca2+通过SOCC内流增强,从而导致大鼠远端PVSMC的[Ca2+]i升高。
[Abstract]:Aim: to investigate the effect of acute hypoxia on the increase of calcium concentration ([Ca2] I) in rat distal pulmonary vein smooth muscle cells induced by Ca2 -ATPase inhibitor cyclopyranilic acid (CPA). Methods: six male Sprague-Dawley rats (body weight 200,250g / g) were used to culture PVSMC. The effects of CPA and acute hypoxia 4O _ 2 on [Ca2] I of PVSMC were observed by fluorescence microscope and intracellular calcium concentration detection system, and chlorine was used as a calcium pool operable calcium channel blocker. The intervention effect of Nickelated Nickelite (NICL _ 2) and SKF96365. Results: Krebs solution containing 5 渭 mol/L nifedipine (voltage-dependent calcium channel blocker) increased [Ca2] I of PVSMC by 10 渭 mol/L CPA, increased [Ca2] I by acute hypoxia, and increased [Ca2] I by 10 渭 mol/L CPA after extracellular Ca2 restoration to 2.5 mmol/L. Acute hypoxia could significantly increase [Ca2] I induced by CPA. Both Ni Cl2(500 渭 mol / L and SKF96365(50 渭 mol / L) inhibited [Ca2] I increase induced by CPA under acute hypoxia, but had no effect on [Ca2] I response induced by hyperkalemia 60 mmol/L KCl)Krebs solution. Conclusion: acute hypoxia can increase [Ca2] I of distal PVSMC induced by CPA, and the increase of [Ca2] I can be blocked by SOCC blocker, suggesting that acute hypoxia can enhance SOCC activity and increase extracellular Ca2 through SOCC influx. Thus, the [Ca2] I of distal PVSMC in rats was increased.
【作者单位】：广州医科大学附属第一医院广州呼吸疾病研究所呼吸疾病国家重点实验室;
【基金】：国家自然科学基金项目(81000020,81570045) 广东省自然科学基金资助项目(2014A030313486) 广州市科技计划资助项目(201510010226) 羊城学者科研计划学术骨干项目(10A025G) 广州市属高校科研项目(10A276) 呼吸疾病国家重点实验室青年科学基金支持项目(11)
【分类号】：R965

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