Mechanisms of hemolysate-induced [Ca2+]i elevation in cerebral smooth muscle cells.
Mechanisms of hemolysate-induced [Ca2+]i elevation in cerebral smooth muscle cells.
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DOI：
10.1152/ajpheart.1995.269.6.h1874
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发表时间：
1995-12
期刊：
影响因子：
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通讯作者：
H. Zhang;B. Weir;L. Marton;R. Macdonald;V. Bindokas;R. Miller;J. Brorson
中科院分区：
文献类型：
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作者：
H. Zhang;B. Weir;L. Marton;R. Macdonald;V. Bindokas;R. Miller;J. Brorson
用Fura 2和双激发波长显微荧光法研究了溶血产物对新鲜分离的大鼠基底动脉平滑肌细胞内游离Ca ~（2+）（[Ca ~（2+）]i）稳态的影响。溶血产物可逆地产生短暂的[Ca 2 +]i峰，随后是缓慢衰减的平台，这在无Ca（2+）溶液中不存在。溶血产物的这种作用被1）肌浆网Ca 2+泵抑制剂毒胡萝卜素和环匹阿尼酸，2）Ca 2+释放阻断剂ryanodine和丹曲林，3）细胞色素P-450抑制剂益康唑，和4）无机钙通道阻滞剂镧，但1）受体调节的钙通道阻滞剂SKF-96365或2）电压依赖性钙通道阻滞剂尼莫地平。使用具有特定孔径（0.5、1和12-14 kDa）的膜对溶血产物进行分级表明，> 0.5但1和> 12-14 kDa的组分产生小而缓慢的[Ca 2 +]i升高，而没有显著的峰。溶血产物中的ATP产生与溶血产物相似的[Ca ~（2+）]i反应。P2-嘌呤受体拮抗剂显著减弱ATP、溶血产物和< 1和< 12-14 kDa的组分的作用。我们的结论是，溶血升高[Ca 2 +]i从内部存储和触发Ca 2+进入，可能从电压依赖性Ca 2+内流途径，效果显然是相同的ATP释放Ca 2+。
The effects of hemolysate on free cytosolic [Ca2+] ([Ca2+]i) homeostasis were studied in freshly isolated rat basilar artery smooth muscle cells using fura 2 and dual excitation wavelength microfluorimetry. Hemolysate reversibly produced a transient [Ca2+]i peak followed by a slowly decaying plateau which was absent in Ca(2+)-free solution. This effect of hemolysate was attenuated by 1) the sarcoplasmic reticulum Ca2+ pump inhibitors thapsigargin and cyclopiazonic acid, 2) the Ca2+ release-blocking agents ryanodine and dantrolene, 3) the cytochrome P-450 inhibitor econazole, and 4) the inorganic Ca2+ channel blocker lanthanum but was not significantly attenuated by 1) the receptor-regulated Ca2+ channel blocker SKF-96365 or 2) the voltage-dependent Ca2+ channel blocker nimodipine. Fractionation of hemolysate using membranes with specific pore sizes (0.5, 1, and 12-14 kDa) indicated that a component(s) > 0.5 but 1 and > 12-14 kDa produced a small and slow [Ca2+]i rise without a significant peak. ATP, which was found in hemolysate, produced a [Ca2+]i response similar to that of hemolysate. P2-purinoceptor antagonists significantly attenuated the effect of ATP, hemolysate, and the fractions < 1 and < 12-14 kDa. We conclude that hemolysate elevates [Ca2+]i by both releasing Ca2+ from internal stores and triggering Ca2+ entry, possibly from a voltage-independent Ca2+ influx pathway, an effect apparently identical to that of ATP.