Ca2+ transients in embryonic chick heart: contributions from Ca2+ channels and the sarcoplasmic reticulum.
Ca2+ transients in embryonic chick heart: contributions from Ca2+ channels and the sarcoplasmic reticulum.
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胚胎鸡心脏中的 Ca2 瞬变：来自 Ca2 通道和肌浆网的贡献。
DOI：
10.1152/ajpheart.1996.270.2.h518
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Creazzo,TL
中科院分区：
文献类型：
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作者：
Brotto,MA;Creazzo,TL
在胚胎哺乳动物心脏中，几乎所有可用于 Ca2+ 瞬态的 Ca2+ 均来自肌膜 Ca2+ 流入。然而，对鸟类的一些研究表明，肌浆网（SR）在发育的相对早期就具有功能。在本报告中，我们研究了来自第 11 天胚胎鸡心脏的单个离体心室肌细胞的场刺激引起的 fura 2 Ca2+ 瞬变，以直接确定 SR 和 Ca2+ 通道的作用。在较高频率的刺激（1 Hz）下观察到正阶梯现象。异丙肾上腺素 (Iso) 以剂量依赖性方式增加瞬态峰值，在 100 µM Iso 中最大增加 93%。硝苯地平 (10 microM) 降低了瞬态，因此在背景噪声之上无法观察到瞬态。然而，当肌细胞受到 Iso 刺激时，Ca2+ 瞬变是可见的。这些被硝苯地平阻断了约 70%，表明大多数（但不是全部）瞬态与 L 型 Ca2+ 电流相关。因此，一部分瞬变可能是由 T 型 Ca2+ 通道和/或反向 Na+/Ca2+ 交换引起的。基于 Ca2+ 电流和细胞体积的积分计算表明，通过肌膜 Ca2+ 通道进入的 Ca2+ 多达四分之一来自 T 型通道。高浓度（10-100 µM）的 Ryanodine 可抑制 30% 的瞬变。 Iso 和兰尼定都缩短了达到峰值的时间、指数衰减的时间常数以及瞬态的总持续时间。当外部溶液含有 1.8 mM CaCl2 时，用高 KCl 去极化肌细胞会引起较大且部分持续的瞬态。外部溶液中的 CaCl2 (10 mM) 引起大的周期性 Ca2+ 振荡。这些结果表明，尽管大多数与瞬时相关的 Ca2+ 通过肌膜 Ca2+ 通道并可能逆转 Na+/Ca2+ 交换，但 SR 在第 22 天孵化之前就在胚胎鸡心脏中发挥了功能。
In the embryonic mammalian heart, virtually all the Ca2+ available for the Ca2+ transient comes through sarcolemmal Ca2+ influx. However, several studies in avian species indicate that the sarcoplasmic reticulum (SR) is functional relatively early in development. For the present report we studied fura 2 Ca2+ transients elicited by field stimulation in single isolated ventricular myocytes from the day 11 embryonic chick heart to ascertain directly the roles of the SR and Ca2+ channels. A positive staircase phenomenon was observed at higher frequencies of stimulation (1 Hz). Isoproterenol (Iso) increased the peak of the transient in a dose-dependent manner with a maximum increase of 93% in 100 microM Iso. Nifedipine (10 microM) reduced the transient such that is was not observable above background noise. However, Ca2+ transients were visible when the myocytes were stimulated by Iso. These were blocked by approximately 70% with nifedipine, suggesting that most, but not all, of the transient is associated with L-type Ca2+ current. Thus a portion of the transient may result from T-type Ca2+ channels and/or reverse Na+/Ca2+ exchange. Calculations based on integration of the Ca2+ currents and cell volume indicate that as much as one-fourth of the Ca2+ entering via sarcolemmal Ca2+ channels is from T-type channels. Ryanodine at high concentrations (10-100 microM) inhibited the transients by 30%. Both Iso and ryanodine reduced the time to peak, the time constant of the exponential decay, and the total duration of the transients. Depolarizing the myocytes with high KCl induced a large and partially sustained transient when the external solution contained 1.8 mM CaCl2. CaCl2 (10 mM) in the external solution induced large cyclic Ca2+ oscillations. These results suggest that the SR is functional in the embryonic chick heart well before hatching at day 22, although most of the Ca2+ associated with the transient comes through the sarcolemmal Ca2+ channels and possibly reverse Na+/Ca2+ exchange.