低氧时钙离子对冠状动脉内皮细胞释放ET-1、NO、PGI2的影响

目的:探讨低氧引起冠状动脉内皮细胞(CAEC)释放ET-1、NO和PGI₂改变的机制。方法:运用放射性⁴⁵Ca²⁺]掺入、放免和比色等方法, 测定常氧组、低氧组冠状动脉内皮细胞钙摄取率, 以及常氧组、低氧组、低氧+维拉帕米组冠状动脉内皮细胞培养液中ET-1、NO和PGI₂含量。结果:低氧组CAEC⁴⁵Ca²⁺]摄取率为(29.6±3.7)ng/gprotein/30min, 常氧对照组为(15.2±1.1)ng/gprotein(P<0.01).低氧+维拉帕米组ET-1分泌量显著多于低氧组(P<0.01).低氧+维拉帕米组分泌的NO显著低于低氧组(P<0.05), 与常氧组相差不显著。低氧+维拉帕米组分泌的PGI₂显著多于低氧组, 与常氧组相差不显著。结论:低氧时引起的NO、ET-1、PGI₂分泌改变与低氧引起的冠状动脉内皮细胞Ca²⁺内流增加有关。

Effects of Ca2+ on the releases of ET-1, NO and PGI2 from bovine coronary artery endothelial cells during hypoxia

AIM: To explore the mechanism of ET-1, NO and PGI 2 release from coronary artery endothelial cells (CAEC) induced by acute hypoxia. METHODS: Bovine coronary artery endothelial cells were cultured and 45 Ca 2+ ] was used to investigate the difference of calcium uptake between normoxia group and hypoxia group (3% O 2). The contents of ET-1, NO and PGI 2 in media of normoxia group, hypoxia group and hypoxia + verapamil group were measured 24 h after hypoxia. RESULTS: 45 Ca 2+ ] uptake by CAEC in hypoxia group was 1.9 times more than normoxia group ( P< 0 01). Hypoxia + verapamil group released more PGI 2, ET-1 and less NO than hypoxia group ( P< 0 05). CONCLUSION: Changes of ET-1, NO and PGI 2 releases during hypoxia may be caused by the inflow of Ca 2+ into coronary artery endothelial cells.