THE RELATIONSHIP BETWEEN CONTRACTILE-FORCE AND INTRACELLULAR [CA2+] IN INTACT RAT CARDIAC TRABECULAE
THE RELATIONSHIP BETWEEN CONTRACTILE-FORCE AND INTRACELLULAR [CA2+] IN INTACT RAT CARDIAC TRABECULAE
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DOI：
10.1085/jgp.105.1.1
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发表时间：
1995-01-01
影响因子：
3.8
通讯作者：
MARBAN, E
中科院分区：
文献类型：
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作者：
BACKX, PH;GAO, WD;MARBAN, E
本文研究了[Ca ~（2+）]对Fura-2盐负载的大鼠心肌小梁的力的控制作用。在肌节长度为2.1-2.3 μ m时，在ryanodine存在下强直化过程中的稳态力-[Ca ~（2+）]（i）关系在[Ca ~（2+）]（i）为0.65 +/- 0.19 μ M时半最大激活，希尔系数为5.2 +/- 1.2（平均值+/- SD，n = 9），饱和[Ca 2 +]（i）时产生的最大应力等于121 +/- 35 mN/mm（2）（n = 9）。稳态力对[Ca ~（2+）]（i）的依赖性在Ca ~（2+）-ATP酶抑制剂环匹阿尼酸（CPA）存在下强直的肌肉中是相同的。在CPA存在下，在抽搐松弛期间的力-[Ca 2 +]（i）关系与强直期间在稳态下测量的完全一致，这表明CPA足以减慢[Ca 2 +]（i）的衰减速率，以使力与[Ca 2 +]（i）进入稳态。相比之下，在对照抽搐的松弛阶段，力与[Ca 2 +]（i）的关系相对于稳态关系发生了显著变化，表明松弛受到收缩系统本身的限制，而不是受到胞质中Ca 2+去除的限制。在对照条件下，力-[Ca 2 +]（i）关系，在峰值抽搐力时定量（即，dF/dt = 0），与某些小梁中的稳态测量相当吻合（即，七分之三）。然而，在峰值力下的力-[Ca 2 +]（i）关系与应用5 mM 2，3-丁二酮单肟（BDM）（以加速跨桥动力学）或100 μ M CPA（以减缓[Ca 2 +]（i）瞬变的弛豫）后的稳态测量不一致。因此，我们的结论是，在生理性抽搐收缩期间力与[Ca 2 +]（i）的关系不能用于预测稳态关系。
The control of force by [Ca2+] was investigated in rat cardiac trabeculae loaded with fura-2 salt. At sarcomere lengths of 2.1-2.3 mu m, the steady state force-[Ca2+](i) relationship during tetanization in the presence of ryanodine was half maximally activated at a [Ca2+](i) of 0.65 +/- 0.19 mu M with a Hill coefficient of 5.2 +/- 1.2 (mean +/- SD, n = 9), and the maximal stress produced at saturating [Ca2+](i) equalled 121 +/- 35 mN/mm(2) (n = 9). The dependence of steady state force on [Ca2+](i) was identical in muscles tetanized in the presence of the Ca2+-ATPase inhibitor cyclopiazonic acid (CPA). The force-[Ca2+](i) relationship during the relaxation of twitches in the presence of CPA coincided exactly to that measured at steady state during tetani, suggesting that CPA slows the decay rate of [Ca2+](i) sufficiently to allow the force to come into a steady state with the [Ca2+](i). In contrast, the relationship of force to [Ca2+](i) during the relaxation phase of control twitches was shifted leftward relative to the steady state relationship, establishing that relaxation is limited by the contractile system itself, not by Ca2+ removal from the cytosol. Under control conditions the force-[Ca2+](i) relationship, quantified at the time of peak twitch force (i.e., dF/dt = 0), coincided fairly well with steady state measurements in some trabeculae (i.e., three of seven). However, the force-[Ca2+](i) relationship at peak force did not correspond to the steady state measurements after the application of 5 mM 2,3-butanedione monoxime (BDM) (to accelerate cross-bridge kinetics) or 100 mu M CPA (to slow the relaxation of the [Ca2+](i) transient). Therefore, we conclude that the relationship of force to [Ca2+](i) during physiological twitch contractions cannot be used to predict the steady state relationship.