The effect of temperature and adrenaline on the relative importance of the sarcoplasmic reticulum in contributing Ca2+ to force development in isolated ventricular trabeculae from rainbow trout
The effect of temperature and adrenaline on the relative importance of the sarcoplasmic reticulum in contributing Ca2+ to force development in isolated ventricular trabeculae from rainbow trout
复制标题
温度和肾上腺素对肌浆网贡献 Ca2 促进虹鳟离体心室小梁发育的相对重要性的影响
DOI：
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发表时间：
1997
影响因子：
2.8
通讯作者：
Anthony P. Farrell
中科院分区：
文献类型：
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作者：
H. Shiels;Anthony P. Farrell
在哺乳动物心脏组织兴奋-收缩（E-C）偶联期间，肌浆网（SR）是细胞内Ca2+调节的中心。在低等脊椎动物中，SR对E-C耦合的重要性尚不确定。这种不确定性可以部分归因于SR Ca2+释放通道的温度依赖性和异温心肌的红嘌呤敏感性的种间差异。此外，SR在促进细胞内Ca2+对力发育的相对重要性可能受到肾上腺素能刺激的影响，肾上腺素能刺激增加了跨肌层（细胞外）Ca2+内流。本研究的目的是评估虹鳟鱼离体心室小梁等距收缩过程中SR（细胞内）和肌层（细胞外）Ca2+通量的相对重要性。为了更好地接近体内Ca2+对肌肉的可利用性，在所有对照实验中都使用了强直水平（10 μ mol l-1）的肾上腺素，并用高水平（10 μ mol l-1）的肾上腺素刺激SL Ca2+内流。Ryanodine是一种著名的哺乳动物SR Ca2+释放阻滞剂，用于评估SR的影响。为了研究温度对每个来源的相对Ca2+贡献的作用，实验在两个温度（12和22°C）下进行，使用来自适应12和22°C的鱼的心室小梁。在所研究的所有测试条件下，通过使用瑞诺定后等长力的变化来评估，SL Ca2+内流是激活剂Ca2+的主要来源。即便如此，激活剂Ca2+的SR贡献在22℃的测试温度下明显大于在12℃的测试温度下。我们将这一观察结果归因于SR Ca2+释放通道的温度依赖性。在22°C和控制条件下，ryanodine降低了所有起搏器频率下的峰值张力（0.2 Hz时约50%，1.2 Hz时约25%，2.0 Hz时约20%），而与驯化温度无关。因此，SR是激活剂Ca2+在温暖温度下张力发展的重要但次要的贡献者。SR Ca2+的贡献大小与起搏频率呈负相关，但在生理起搏频率下仍然显著。这是一个新颖的发现。在本研究中，虹鳟鱼对ryanoine的敏感程度比以前报道的要高。我们将这种差异归因于本研究中强直性肾上腺素能刺激的使用。与在12°C和控制条件下的较热测试温度下的实验相比，无论驯化温度如何，ryanodine仅在低频时显著降低峰值张力（0.2 Hz时约25%）。这些发现表明，在低温和生理相关的起搏频率下，SR在向鳟鱼心脏的收缩元素提供Ca2+方面可能并不重要。在两种测试温度下，无论驯化温度如何，10µmol l-1肾上腺素刺激引起的正性肌力足以完全改善ryanodine的负性肌力效应，但22°C的高起搏频率（>1.2 Hz）除外，肾上腺素能刺激不能完全补偿ryanodine的作用。这一例外是讨论有关降低肾上腺素能敏感性的鳟鱼心肌在温暖的温度。肾上腺素能介导的对SR Ca2+供应损失的补偿是鱼心脏的新发现。因此，尽管我们的研究清楚地表明SR Ca2+释放的相对重要性受温度和频率的影响，肾上腺素介导的SL Ca2+内流的增加降低了SR在促进Ca2+对鳟鱼心室肌丝E-C偶联中的重要性。
The sarcoplasmic reticulum (SR) is central to intracellular Ca2+ regulation during excitationcontraction (E-C) coupling in mammalian cardiac tissue. The importance of the SR to E-C coupling in lower vertebrates is less certain. This uncertainty can be attributed, in part, to the temperature-dependency of the SR Ca2+-release channel and to interspecific differences in the ryanodine-sensitivity of ectotherm cardiac muscle. Furthermore, the relative importance of the SR in contributing intracellular Ca2+ to force development may be influenced by adrenergic stimulation, which increases trans-sarcolemmal (extracellular) Ca2+ influx. The objective of this study was to assess the relative importance of SR (intracellular) and sarcolemmal (SL; extracellular) Ca2+ fluxes during the isometric contraction of isolated ventricular trabeculae from rainbow trout Oncorhynchus mykiss. To approximate in vivo Ca2+ availability to the muscle better, a tonic level (10 nmol l-1) of adrenaline was used in all control experiments, and SL Ca2+ influx was stimulated with high levels (10 µmol l-1) of adrenaline. Ryanodine, a noted blocker of SR Ca2+ release in mammals, was used to assess SR involvement. To examine the role of temperature on the relative Ca2+ contribution from each source, experiments were performed at two temperatures (12 and 22 °C), using ventricular trabeculae from fish acclimated to both 12 and 22 °C. Under all test conditions studied, SL Ca2+ influx was the primary source of activator Ca2+, as assessed by the change in isometric force after ryanodine application. Even so, the SR contribution of activator Ca2+ was significantly greater at a test temperature of 22 °C than at 12 °C. We attribute this observation to the temperature-dependent nature of the SR Ca2+-release channel. At 22 °C and under control conditions, ryanodine reduced peak tension at all pacing frequencies (by approximately 50 % at 0.2 Hz, approximately 25 % at 1.2 Hz and approximately 20 % at 2.0 Hz), regardless of acclimation temperature. Therefore, the SR is a significant, but secondary, contributor of activator Ca2+ for tension development at warm temperatures. The magnitude of SR Ca2+ contribution was inversely related to pacing frequency, but remained significant at physiological pacing frequencies. This was a novel finding. The degree of ryanodine-sensitivity in the present study was greater than that reported previously for the rainbow trout. We attribute this difference to the use of tonic adrenergic stimulation in the present study. In contrast to the experiments at the warmer test temperature, at 12 °C and under control conditions, ryanodine significantly reduced peak tension only at low frequencies (by approximately 25 % at 0.2 Hz), regardless of acclimation temperature. These findings suggest that at cold temperatures, and at physiologically relevant pacing frequencies, the SR may not be important in supplying Ca2+ to the contractile elements of the trout heart. At both test temperatures and regardless of acclimation temperature, stimulation with 10 µmol l-1 adrenaline caused positive inotropy of sufficient magnitude to ameliorate the negative inotropic effect of ryanodine completely, with the exception of high pacing frequencies (>1.2 Hz) at 22 °C, where adrenergic stimulation did not fully compensate for the effects of ryanodine. This exception is discussed in relation to the reduced adrenergic sensitivity of the trout myocardium at warm temperatures. The adrenergically mediated compensation for the loss of the SR Ca2+ supply is a novel finding for fish hearts. Therefore, while our study clearly demonstrates that the relative importance of SR Ca2+ release is subject to temperature and frequency, adrenaline-mediated increases in SL Ca2+ influx decrease the importance of the SR in contributing Ca2+ to E-C coupling in trout ventricular myofilaments.
影响因子：
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作者：
ROUSSEAU, E;SMITH, JS;MEISSNER, G
通讯作者：
MEISSNER, G