Hyperglycemia alters cytoplasmic Ca2+ responses to capacitative Ca2+ influx in rat aortic smooth muscle cells.
Hyperglycemia alters cytoplasmic Ca2+ responses to capacitative Ca2+ influx in rat aortic smooth muscle cells.
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高血糖改变大鼠主动脉平滑肌细胞中细胞质 Ca2 对电容性 Ca2 流入的反应。
DOI：
10.1152/ajpcell.1995.269.6.c1482
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Marchase,RB
中科院分区：
文献类型：
--
作者：
Rivera,AA;White,CR;Guest,LL;Elton,TS;Marchase,RB
用比率钙指示剂呋喃2-乙酰氧基甲酯（AM）监测大鼠主动脉平滑肌（RASM）细胞胞浆游离钙浓度。在5 mM葡萄糖中培养的RASM细胞中，与血管紧张素II、ATP或毒胡萝卜素[肌浆网（SR）Ca（2+）-ATP酶的选择性抑制剂]孵育可耗尽SR Ca 2+储存，并启动通过质膜的容量性Ca 2+内流。这种内流对维拉帕米（L型电压门控Ca 2+通道的选择性抑制剂）具有抗性，但对SKF-96365（受体操纵的Ca 2+进入途径的抑制剂）敏感。RASM细胞培养在25 mM葡萄糖表现出显着减少胞质Ca 2+反应激动剂诱导的Ca 2+释放SR存储和随后的容量Ca 2+进入。此外，高血糖细胞中对毒胡萝卜素诱导的SR中Ca 2+释放的细胞质反应比对照细胞更急剧地达到峰值，并更快地恢复到基线。高血糖的影响并没有克服肌醇补充。
Concentrations of free cytoplasmic Ca2+ in rat aortic smooth muscle (RASM) cells were monitored using the ratiometric Ca2+ indicator fura 2-acetoxymethyl ester (AM). In RASM cells cultured in 5 mM Glc, incubation with angiotensin II, ATP, or thapsigargin [a selective inhibitor of the sarcoplasmic reticulum (SR) Ca(2+)-ATPase] depleted SR Ca2+ stores and initiated a capacitative Ca2+ influx through the plasma membrane. This influx was resistant to verapamil, a selective inhibitor of L-type voltage-gated Ca2+ channels, but was sensitive to SKF-96365, an inhibitor of the receptor-operated Ca2+ entry pathway. RASM cells cultured in 25 mM Glc exhibited a significant decrease in cytoplasmic Ca2+ responses to agonist-induced Ca2+ release from SR stores and to subsequent capacitative Ca2+ entry. In addition, the cytoplasmic response to thapsigargin-induced release of Ca2+ from the SR in hyperglycemic cells peaked more sharply than in control cells and returned to baseline more rapidly. The effects of hyperglycemia were not overcome by myo-inositol supplementation.