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α-肾上腺素能介导的Ca2+流入心脏线粒体的激活。一种调节线粒体内游离Ca2+的可能机制。

The alpha-adrenergic-mediated activation of Ca2+ influx into cardiac mitochondria. A possible mechanism for the regulation of intramitochondrial free CA2+.

作者信息

Kessar P, Crompton M

出版信息

Biochem J. 1981 Nov 15;200(2):379-88. doi: 10.1042/bj2000379.

Abstract

Mitochondria isolated from rat hearts perfused with adrenaline, and from hearts excised from adrenaline-treated rats, showed an enhanced rate of respiration-dependent Ca2+ uptake. Adrenaline pretreatment did not change the activity of the Na+/Ca2+-antiporter of isolated heart mitochondria. Simultaneous measurements of the membrane potential revealed that perfusion with adrenaline has no significant effect on this parameter during Ca2+ accumulation. The activation of Ca2+ uptake was induced also by the alpha-adrenergic agonist, methoxamine, but not by the beta-adrenergic agonist, isoprenaline. Methoxamine pretreatment also increased the sensitivity of alpha-oxoglutarate dehydrogenase in intact mitochondria to 10 nM--300 nM extramitochondrial Ca2+ during steady-state Ca2+ recycling across the inner membrane. Possible implications of these data for the adrenergic regulation of oxidative metabolism are discussed.

摘要

从用肾上腺素灌注的大鼠心脏以及从经肾上腺素处理的大鼠身上切除的心脏中分离出的线粒体,显示出呼吸依赖性Ca2+摄取速率增强。肾上腺素预处理并未改变分离的心脏线粒体中Na+/Ca2+反向转运体的活性。同时测量膜电位发现,在Ca2+积累过程中,用肾上腺素灌注对该参数没有显著影响。α-肾上腺素能激动剂甲氧明也可诱导Ca2+摄取的激活,但β-肾上腺素能激动剂异丙肾上腺素则不能。在稳态Ca2+跨内膜循环过程中,甲氧明预处理还增加了完整线粒体中α-酮戊二酸脱氢酶对10 nM - 300 nM线粒体外Ca2+的敏感性。讨论了这些数据对肾上腺素能调节氧化代谢的可能影响。

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