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Effects of hypoxia and mitochondrial inhibition on the capacitative calcium entry in rabbit pulmonary arterial smooth muscle cells.

机译:低氧和线粒体抑制作用对家兔肺动脉平滑肌细胞中钙离子进入能力的影响。

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We have investigated the effects of hypoxia and mitochondria inhibitors on the capacitative Ca(2+) entry (CCE) in cultured smooth muscle cells from rabbit small pulmonary arteries. Cyclopiazonic acid (CPA) depleted Ca(2+) from sarcoplasmic reticulum (SR) in Ca(2+)-free medium and subsequent addition of Ca(2+) led to the nifedipine-insensitive, La(3+)-sensitive Ca(2+) influx. The presence of CCE was further verified by the measurement of unidirectional Mn(2+) influx. During the decay phase of the CCE-induced [Ca(2+)]c transients, hypoxia (P(O2) < 50 mmHg) and the mitochondria inhibitor FCCP reversibly increased [Ca(2+)]c, that is La(3+)-sensitive. Once SR is depleted by CPA, subsequent treatment of FCCP slowed the decay of CCE-induced [Ca(2+)]c transients but it did not attenuate Mn(2+) influx. Mitochondrial uptake of incoming Ca(2+) through CCE was demonstrated by additional increase in [Ca(2+)]c with Ca(2+) ionophore after terminating CCE. Together, it is suggested that the augmentation of CCE-induced[Ca(2+)]c transients by hypoxia and FCCP reflects a net gain of [Ca(2+)]c by the inhibition of mitochondrial Ca(2+) uptake.
机译:我们已经研究了缺氧和线粒体抑制剂对兔小肺动脉培养的平滑肌细胞中能性Ca(2+)进入(CCE)的影响。 Cyclopiazonic酸(CPA)从无Ca(2+)的肌浆网(SR)中耗尽Ca(2+),随后添加Ca(2+)导致硝苯地平不敏感,La(3+)敏感的Ca (2+)涌入。 CCE的存在通过单向Mn(2+)流入的测量进一步验证。在CCE诱导的[Ca(2 +)] c瞬变的衰减阶段,缺氧(P(O2)<50 mmHg)和线粒体抑制剂FCCP可逆地增加[Ca(2 +)] c,即La(3) +)敏感。一旦SR被CPA消耗掉,FCCP的后续处理就减缓了CCE诱导的[Ca(2 +)] c瞬变的衰减,但并未减弱Mn(2+)的流入。终止CCE后,通过Ca(2+)离子载体的[Ca(2 +)] c的额外增加证明了通过CCE传入Ca(2+)的线粒体摄取。在一起,建议缺氧和FCCP CCE诱导的[Ca(2 +)] c瞬态的增加反映了通过抑制线粒体Ca(2+)摄取的[Ca(2 +)] c的净收益。

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