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钠钙交换对于兔和大鼠心室肌细胞收缩的静息衰减是必需的,但对于收缩的静息增强并非必需。

Na-Ca exchange is required for rest-decay but not for rest-potentiation of twitches in rabbit and rat ventricular myocytes.

作者信息

Bassani R A, Bers D M

机构信息

Department of Physiology, Loyola University School of Medicine, Maywood, IL 60153.

出版信息

J Mol Cell Cardiol. 1994 Oct;26(10):1335-47. doi: 10.1006/jmcc.1994.1152.

DOI:10.1006/jmcc.1994.1152
PMID:7869394
Abstract

The influence of the Na-Ca exchange (NaCaX) on the effects of rest (30-300 s) on twitch amplitude and SR Ca content (assessed by caffeine contractures) was studied in ventricular myocytes isolated from rat and rabbit. In control conditions, rabbit cells showed monotonic rest-decay of the amplitudes of both twitch and caffeine contractures, while rat myocytes developed rest-potentiation of twitches without change in SR Ca content. Inhibition of the Na-Ca exchange during rest by perfusion with 0Na,0Ca solution did not affect the responses in rat cells but abolished rest-dependent SR Ca loss in rabbit cells. Indeed, when NaCaX was blocked during rest, then rabbit cells, like rat, displayed rest-potentiation of twitches. Stimulation of net Ca extrusion via NaCaX during rest by perfusion with 0Ca solution induced rest-decay of twitches and caffeine contractures in rat cells similar to that observed in rabbit cells. This maneuver also accelerated decline in SR Ca during rest and amplitude of the first post-rest twitch in rabbit myocytes. These effects were only slightly enhanced by preperfusion with 0Na,0Ca solution to deplete Nai. We were thus able to interconvert the contractile responses to rest between these cell types solely by modifying the driving force for Ca transport by the exchange. Our results indicate that SR Ca is lost during quiescence in both species, but only if the NaCaX is able to promote diastolic Ca extrusion will net decline of SR Ca (and twitch amplitude) occur. On the other hand, post-rest twitch potentiation in both rat and rabbit cells can occur without a change in SR Ca content. This effects might be attributable, at least in part, to a slow phase of recovery of excitation-contraction coupling.

摘要

在从大鼠和兔子分离出的心室肌细胞中,研究了钠钙交换(NaCaX)对静息(30 - 300秒)对抽搐幅度和肌浆网(SR)钙含量(通过咖啡因收缩来评估)的影响。在对照条件下,兔细胞的抽搐和咖啡因收缩幅度均呈现单调的静息衰减,而大鼠心肌细胞的抽搐出现静息增强,且SR钙含量无变化。在静息期间用无钠、无钙溶液灌注抑制钠钙交换,对大鼠细胞的反应没有影响,但消除了兔细胞中依赖于静息的SR钙流失。实际上,当在静息期间阻断NaCaX时,兔细胞和大鼠细胞一样,抽搐出现静息增强。在静息期间用无钙溶液灌注刺激通过NaCaX的净钙外排,诱导大鼠细胞的抽搐和咖啡因收缩出现静息衰减,类似于在兔细胞中观察到的情况。这种操作还加速了兔心肌细胞静息期间SR钙的下降以及静息后首次抽搐的幅度。预先用无钠、无钙溶液灌注以耗尽细胞内钠(Nai),这些效应仅略有增强。因此,我们仅通过改变交换体对钙转运的驱动力,就能在这些细胞类型之间相互转换对静息的收缩反应。我们的结果表明,在这两个物种中,静止期SR钙都会流失,但只有当NaCaX能够促进舒张期钙外排时,SR钙(和抽搐幅度)才会出现净下降。另一方面,大鼠和兔细胞的静息后抽搐增强可以在SR钙含量不变的情况下发生。这种效应可能至少部分归因于兴奋 - 收缩偶联恢复的缓慢阶段。

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