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Influence of the 15-HETE on cytosolic [ Ca2+] i of the rabbit pulmonary artery smooth muscle cells

机译:15-HETE对家兔肺动脉平滑肌细胞胞质[Ca2 +] i的影响

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Extracellular Ca2+ influx was blocked by L-type Ca2+ channel blocker nifedipine to observe the effects of 15-hydroxyeicosatetraenoic acid on the constriction of rabbit pulmonary artery rings and on the changes of Ca2+ level in the rabbit pulmonary artery smooth muscle cells, and further to investigate the mechanism of the calcium mobilization induced by the 15-HETE under hypoxic conditions. The effect of extracellular Ca2+ on tension of the rabbit PA rings was also studied. Nifedipine (10 μ mol/L) had no effect on 1 μ mol/L 15-hydroxyeicosatetraenoic acid induced vasoconstriction under normoxic and hypoxic conditions. Intracellular Ca2+ increased markedly in the 15-HETE group (cells were exposed to 1 μ mol/L 15-HETE for 8 min during culture) compared to the control group (P < 0.05). The study demonstrated that the 15-HETE could induce the elevation of Ca2+ in the pulmonary artery smooth muscle cells and the elevated calcium came from the release of the intracellular calcium.
机译:用L型Ca2 +通道阻滞剂硝苯地平阻断细胞外Ca2 +内流,观察15-羟基二十碳四烯酸对兔肺动脉环收缩和家兔肺动脉平滑肌细胞Ca2 +水平变化的影响,并进一步研究在低氧条件下由15-HETE引起的钙动员机制。还研究了细胞外Ca2 +对兔PA环张力的影响。硝苯地平(10μmol / L)在常氧和低氧条件下对1μmol/ L 15-羟基二十碳四烯酸诱导的血管收缩没有影响。与对照组相比,15-HETE组的细胞内Ca2 +显着增加(细胞在培养过程中暴露于1μmol / L 15-HETE 8分钟)(P <0.05)。研究表明15-HETE可以诱导肺动脉平滑肌细胞中Ca2 +的升高,而钙的升高则来自细胞内钙的释放。

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