Maximal Ca2+‐Activated Force Elicited by Tetanization Ferret Papillary Muscle and Whole Heart: Mechanism and Characteristics of Steady Contractile Activation in Intact Myocardium
Maximal Ca2+‐Activated Force Elicited by Tetanization Ferret Papillary Muscle and Whole Heart: Mechanism and Characteristics of Steady Contractile Activation in Intact Myocardium
复制标题
强直刺激雪貂乳头肌和整个心脏引起的最大 Ca2+ 激活力：完整心肌稳定收缩激活的机制和特征
作者：
E. Marbán;H. Kusuoka;D. T. Yue;M. Weisfeldt;W. Wier
用ryanodine处理的完整心肌的快速（8-12 Hz）刺激导致称为强直的稳定收缩激活，其幅度可以通过改变细胞外Ca 2+浓度（[Ca 2 +]0）来分级。在雪貂乳头肌中，通过测量膜电位和通过测定力和细胞内游离Ca 2+浓度（[Ca 2 +]i，用水母发光蛋白估计）对二氢吡啶Ca通道配体的响应性来探索持续力产生的机制。强直时的膜电位介于− 25至− 60 mV之间，表明快或慢钙通道或钠钙交换可能介导钙离子进入。二氢吡啶效应表明慢钙通道起主要作用：激动剂Bay K 8644（0.3-1 μM）增加力和水母发光，而拮抗剂尼群地平（1-30 μM）消除强直。在类似于乳头肌实验的条件下，暴露于ryanodine后，在整个Langendorff灌注的雪貂心脏中产生破伤风。收缩饱和作为乳头肌和整个心脏中[Ca 2 +]0的函数;即，当[Ca 2 +]0增加到10 mM以上时，力或压力产生没有进一步增加。相比之下，在乳头肌中测量的水母发光蛋白发光显示没有这种饱和。因此，在[Ca 2 +] 0 ± 10 mM强直期间实现了最大Ca 2+激活力（或压力）。在整个心脏（15 mM [Ca 2 +]0）强直期间壁应力的计算与乳头肌中最大张力的直接测量结果（分别为5.84 g/mm 2和6.41 g/mm 2）一致。我们的结论是，最大的钙激活力（或压力），可以产生在强直在高[Ca 2 +]0在整个心脏或孤立的乳头肌暴露于ryanodine。
Rapid (8–12 Hz) stimulation of intact heart muscle treated with ryanodine results in steady contractile activation known as tetanus, the amplitude of which can be graded by changing extracellular Ca2+ concentration ([Ca2+]0). The mechanism of the sustained force generation was explored in ferret papillary muscles by measuring membrane potential and by determining the responsiveness of force and intracellular free Ca2+ concentration ([Ca2+]i, estimated with aequorin) to dihydropyridine Ca channel ligands. Membrane potential during tetani ranged from − 25 to − 60 mV, suggesting that fast or slow Ca channels, or Na-Ca exchange, might be mediating Ca2+ entry. Dihydropyridine effects indicated that slow Ca channels play a predominant role: The agonist Bay K 8644 (0.3-1 μM) increased force and aequorin luminescence, whereas the antagonist nitrendipine (1–30 μM) abolished the tetanus. Under conditions analogous to those in the papillary muscle experiments, tetani were produced in whole Langendorff-perfused ferret hearts following exposure to ryanodine. Contraction saturated as a function of [Ca2+]0 in both papillary muscles and whole hearts; i.e., as [Ca2+]0 was increased above 10 mM, no further increase in force or pressure generation occurred. In contrast, aequorin luminescence measured in the papillary muscles showed no such saturation. Thus, maximal Ca2+-activated force (or pressure) was achieved during tetani at [Ca2+]o ± 10 mM. Calculations of wall stress during tetani in whole heart (15 mM [Ca2+]0) agree well with direct measurements of maxima] tension in papillary muscles (5.84 g/mm2 vs. 6.41 g/mm2, respectively). We conclude that maximal Ca2+-activated force (or pressure) can be produced during tetani at high [Ca2+]0 in either whole hearts or isolated papillary muscles following exposure to ryanodine.
心脏收缩蛋白的调节。
影响因子：
20.1
作者：
Winegrad,S
通讯作者：
Winegrad,S
影响因子：
3.4
作者：
ROBERTSON, SP;JOHNSON, JD;POTTER, JD
通讯作者：
POTTER, JD
哺乳动物心室肌中的钙瞬变。
影响因子：
39.3
作者：
Allen,DG;Kurihara,S
通讯作者：
Kurihara,S