Effects of hypoxia and mitochondrial inhibition on the capacitative calcium entry in rabbit pulmonary arterial smooth muscle cells
Effects of hypoxia and mitochondrial inhibition on the capacitative calcium entry in rabbit pulmonary arterial smooth muscle cells
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DOI：
10.1016/s0024-3205(02)02441-4
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发表时间：
2003-02-14
期刊：
影响因子：
6.1
通讯作者：
Uhm, DY
中科院分区：
文献类型：
--
作者：
Kang, TM;Park, MK;Uhm, DY
我们观察了低氧和线粒体抑制剂对培养的兔小肺动脉平滑肌细胞电容性钙内流(CCE)的影响。在无钙介质中，环匹阿松酸(CPA)耗尽肌浆网(SR)中的钙离子，随后钙离子的加入导致硝苯地平不敏感、La3+敏感的钙离子内流。通过测量Mn2+的单向内流，进一步证实了CCE的存在。在CCE诱导的[Ca~(2+)]C瞬变的衰减期，低氧(P-O_2和50 mm Hg)和线粒体抑制剂FCCP可逆地使[Ca~(2+)]C升高，即对La~(3+)敏感。一旦肌浆网被CPA耗尽，随后的FCCP处理减缓了CCE诱导的[Ca~(2+)]C瞬变的衰减，但它没有减弱Mn2+的内流。在终止CCE后，线粒体通过CCE对进入的钙离子的摄取表现为[Ca~(2+)]C和钙离子载体的额外增加。综上所述，缺氧和FCCP对CCE诱导的[Ca~(2+)]_c瞬变的增强反映了通过抑制线粒体Ca~(2+)摄取而导致的[Ca~(2+)]_c的净获得。(C)2002 Elsevier Science Inc.保留所有权利。
We have investigated the effects of hypoxia and mitochondria inhibitors on the capacitative Ca2+ entry (CCE) in cultured smooth muscle cells from rabbit small pulmonary arteries. Cyclopiazonic acid (CPA) depleted Ca2+ from sarcoplasmic reticulum (SR) in Ca2+-free medium and subsequent addition of Ca2+ led to the nifedipine-insensitive, La3+-sensitive Ca2+ influx. The presence of CCE was further verified by the measurement of unidirectional Mn2+ influx. During the decay phase of the CCE-induced [Ca2+]C transients, hypoxia (P-O2 < 50 mmHg) and the mitochondria inhibitor FCCP reversibly increased [Ca2+]C, that is La3+-sensitive. Once SR is depleted by CPA, subsequent treatment of FCCP slowed the decay of CCE-induced [Ca2+]C transients but it did not attenuate Mn2+ influx. Mitochondrial uptake of incoming Ca2+ through CCE was demonstrated by additional increase in [Ca2+]C with Ca2+ ionophore after terminating CCE. Together, it is suggested that the augmentation of CCE-induced [Ca2+]C transients by hypoxia and FCCP reflects a net gain of [Ca2+]c by the inhibition of mitochondrial Ca2+ uptake. (C) 2002 Elsevier Science Inc. All rights reserved.