Shattock M J, Bers D M
Division of Biomedical Sciences, University of California, Riverside 92521-0121.
Am J Physiol. 1989 Apr;256(4 Pt 1):C813-22. doi: 10.1152/ajpcell.1989.256.4.C813.
Trans sarcolemmal Ca movements in rabbit and rat ventricular muscle were compared using extracellular double-barreled Ca-selective microelectrodes. In rabbit ventricle, steady-state twitches were associated with transient extracellular Ca (Cao) depletions, indicative of Ca uptake during the twitch. In contrast, steady-state twitches in rat ventricle were associated with net cellular Ca extrusion. Rest periods in rabbit ventricle lead to a net loss of cell Ca and resumption of stimulation induces a net uptake of Ca by the cells. Conversely, in rat ventricle rest periods lead to cellular Ca gain and resumption of stimulation induces a net Ca loss from the cells. Thus stimulation is associated with net Ca gain in rabbit ventricle and net Ca loss in rat ventricle. These observations provide an explanation for some of the functional differences between rat and rabbit ventricle (e.g., negative force-frequency staircase and rest potentiation in rat vs. positive staircase and rest decay in rabbit). Resting intracellular Na activity (alpha iNa) was 12.7 +/- 0.6 mM in rat and 7.2 +/- 0.5 mM in rabbit ventricle. This alpha iNa in rat ventricle is sufficiently high that Ca entry via Na-Ca exchange is thermodynamically favored at the resting membrane potential. This may explain why rest potentiation is observed in rat ventricle. In contrast, the lower alpha iNa in rabbit ventricle would favor Ca extrusion via Na-Ca exchange at rest (and consequent rest decay). In rat ventricle, the increase of intracellular [Ca] ([Ca]i) associated with contraction, coupled with the short action potential duration, strongly favor Ca extrusion via Na-Ca exchange and explain the observed Cao accumulation observed during twitches in rat. The high plateau of the rabbit ventricular action potential tends to prevent Ca extrusion via Na-Ca exchange during the contraction and explains the Cao depletions observed in rabbit. It is concluded that the higher alpha iNa and shorter action potential duration in rat vs. rabbit ventricle can explain many of the functional differences observed in these tissues.
使用细胞外双管钙选择性微电极比较了兔和大鼠心室肌中的跨肌膜钙运动。在兔心室中，稳态抽搐与短暂的细胞外钙（Cao）消耗有关，这表明抽搐期间有钙摄取。相反，大鼠心室中的稳态抽搐与细胞钙的净外排有关。兔心室的静息期导致细胞钙的净损失，而刺激的恢复则诱导细胞对钙的净摄取。相反，在大鼠心室中，静息期导致细胞钙增加，刺激的恢复则诱导细胞钙的净损失。因此，刺激与兔心室中钙的净增加和大鼠心室中钙的净损失有关。这些观察结果为大鼠和兔心室之间的一些功能差异提供了解释（例如，大鼠中的负力-频率阶梯和静息增强与兔中的正阶梯和静息衰减）。大鼠心室中的静息细胞内钠活性（αiNa）为12.7±0.6 mM，兔心室中为7.2±0.5 mM。大鼠心室中的这种αiNa足够高，以至于在静息膜电位下通过钠-钙交换的钙内流在热力学上是有利的。这可能解释了为什么在大鼠心室中观察到静息增强。相反，兔心室中较低的αiNa有利于静息时通过钠-钙交换的钙外排（以及随之而来的静息衰减）。在大鼠心室中，与收缩相关的细胞内[Ca]（[Ca]i）增加，加上短动作电位持续时间，强烈有利于通过钠-钙交换的钙外排，并解释了在大鼠抽搐期间观察到的Cao积累。兔心室动作电位的高原期往往会在收缩期间阻止通过钠-钙交换的钙外排，并解释了在兔中观察到的Cao消耗。结论是，与兔心室相比，大鼠心室中较高的αiNa和较短的动作电位持续时间可以解释在这些组织中观察到的许多功能差异。
