Hu Q H, Wang D X
Department of Pathophysiology, Tongji Medical University, Wuhan.
J Tongji Med Univ. 1994;14(4):200-3. doi: 10.1007/BF02897667.
By using Ca(2+)-sensitive fluorescent probe, Fura- 2, the effects of endothelial cell-conditioned medium and hypoxia on intracellular free calcium ([Ca2+]i) in cultured pulmonary artery smooth muscle cell (PASMC) were studied. Normoxic porcine pulmonary artery endothelial cell-conditioned medium (NPAECCM) obviously elevated [Ca2+]i in PASMC, whereas the hypoxic porcine pulmonary artery endothelial cell conditioned medium (HPAECCM) significantly elevated [Ca2+]i in PASMC much more than NPAECCM. Both the effects of NPAECCM and HPAECCM were dependent on the cultured endothelial cell extracellular calcium concentrations, ranged from 1.8 mmol/L to 2.4 mmol/L. Meanwhile, hypoxia directly increased, which was partially inhibited by verapamil, [Ca2+]i in PASMC through Ca2+ influx pathway. The data suggest that the augmented regulation of endothelial cell on PASMC via Ca2+ second messenger system and the hypoxia-induced Ca2+ influx into PASMC, particularly the former, may be components of mechanisms underlying hypoxic pulmonary vasoconstriction and chronic pulmonary hypertension.
通过使用钙敏感荧光探针Fura-2，研究了内皮细胞条件培养基和缺氧对培养的肺动脉平滑肌细胞（PASMC）内游离钙（[Ca2+]i）的影响。常氧猪肺动脉内皮细胞条件培养基（NPAECCM）可显著升高PASMC中的[Ca2+]i，而缺氧猪肺动脉内皮细胞条件培养基（HPAECCM）使PASMC中的[Ca2+]i升高幅度明显大于NPAECCM。NPAECCM和HPAECCM的作用均依赖于培养的内皮细胞外钙浓度，范围为1.8 mmol/L至2.4 mmol/L。同时，缺氧直接增加PASMC中的[Ca2+]i，维拉帕米可部分抑制该作用，缺氧通过Ca2+内流途径增加[Ca2+]i。这些数据表明，内皮细胞通过Ca2+第二信使系统对PASMC的调节增强以及缺氧诱导Ca2+流入PASMC，尤其是前者，可能是缺氧性肺血管收缩和慢性肺动脉高压潜在机制的组成部分。
