NA-CA EXCHANGE IS REQUIRED FOR REST-DECAY BUT NOT FOR REST-POTENTIATION OF TWITCHES IN RABBIT AND RAT VENTRICULAR MYOCYTES
NA-CA EXCHANGE IS REQUIRED FOR REST-DECAY BUT NOT FOR REST-POTENTIATION OF TWITCHES IN RABBIT AND RAT VENTRICULAR MYOCYTES
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DOI：
10.1006/jmcc.1994.1152
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发表时间：
1994-10-01
影响因子：
5
通讯作者：
BERS, DM
中科院分区：
文献类型：
--
作者：
BASSANI, RA;BERS, DM
在从大鼠和兔子分离的心室肌细胞中研究了钠钙交换 (NaCaX) 对休息（30-300 秒）对抽搐幅度和 SR Ca 含量（通过咖啡因挛缩评估）的影响。在对照条件下，兔细胞表现出抽搐和咖啡因挛缩幅度的单调静止衰减，而大鼠肌细胞则出现抽搐的静止增强，而 SR Ca 含量没有变化。通过灌注 ONa、OCa 溶液抑制休息期间的 Na-Ca 交换不会影响大鼠细胞的反应，但消除了兔细胞中依赖于休息的 SR Ca 损失。事实上，当 NaCaX 在休息期间被阻断时，兔子细胞像大鼠一样，表现出抽搐的休息增强。在静息期间，通过灌注 OCa 溶液，通过 NaCaX 刺激净 Ca 排出，诱导大鼠细胞中抽搐和咖啡因挛缩的静息衰退，与在兔细胞中观察到的情况类似。这种操作还加速了兔子肌细胞休息期间 SR Ca 的下降以及第一次休息后抽搐幅度的下降。通过预灌注 ONa、OCa 溶液以消耗 Na-i，这些效果仅略有增强。因此，我们能够仅通过改变交换的 Ca 运输驱动力来将这些细胞类型之间的收缩反应相互转换为休息。我们的结果表明，两个物种在静止期间 SR Ca 都会丢失，但只有当 NaCaX 能够促进舒张期 Ca 排出时，SR Ca（和抽搐幅度）才会发生净下降。另一方面，大鼠和兔细胞的静息后抽搐增强可以在 SR Ca 含量不发生变化的情况下发生。这种效应可能至少部分归因于兴奋-收缩耦合恢复的缓慢阶段。
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 ONa,OCa 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 OCa 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 ONa,OCa solution to deplete Na-i. 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.