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首页> 外文期刊>Brazilian Journal of Medical and Biological Research >Effect of exercise training on Ca2+ release units of left ventricular myocytes of spontaneously hypertensive rats
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Effect of exercise training on Ca2+ release units of left ventricular myocytes of spontaneously hypertensive rats

机译：运动训练对自发性高血压大鼠左室心肌细胞钙离子释放单位的影响

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In cardiomyocytes, calcium (Ca2+) release units comprise clusters of intracellular Ca2+ release channels located on the sarcoplasmic reticulum, and hypertension is well established as a cause of defects in calcium release unit function. Our objective was to determine whether endurance exercise training could attenuate the deleterious effects of hypertension on calcium release unit components and Ca2+ sparks in left ventricular myocytes of spontaneously hypertensive rats. Male Wistar and spontaneously hypertensive rats (4 months of age) were divided into 4 groups: normotensive (NC) and hypertensive control (HC), and normotensive (NT) and hypertensive trained (HT) animals (7 rats per group). NC and HC rats were submitted to a low-intensity treadmill running protocol (5 days/week, 1 h/day, 0% grade, and 50-60% of maximal running speed) for 8 weeks. Gene expression of the ryanodine receptor type 2 (RyR2) and FK506 binding protein (FKBP12.6) increased (270%) and decreased (88%), respectively, in HC compared to NC rats. Endurance exercise training reversed these changes by reducing RyR2 (230%) and normalizing FKBP12.6 gene expression (112%). Hypertension also increased the frequency of Ca2+ sparks (HC=7.61±0.26 vs NC=4.79±0.19 per 100 μm/s) and decreased its amplitude (HC=0.260±0.08 vs NC=0.324±0.10 ΔF/F0), full width at half-maximum amplitude (HC=1.05±0.08 vs NC=1.26±0.01 μm), total duration (HC=11.51±0.12 vs NC=14.97±0.24 ms), time to peak (HC=4.84±0.06 vs NC=6.31±0.14 ms), and time constant of decay (HC=8.68±0.12 vs NC=10.21±0.22 ms). These changes were partially reversed in HT rats (frequency of Ca2+ sparks=6.26±0.19 μm/s, amplitude=0.282±0.10 ΔF/F0, full width at half-maximum amplitude=1.14±0.01 μm, total duration=13.34±0.17 ms, time to peak=5.43±0.08 ms, and time constant of decay=9.43±0.15 ms). Endurance exercise training attenuated the deleterious effects of hypertension on calcium release units of left ventricular myocytes.
机译：在心肌细胞中，钙（Ca2 +）释放单元包括位于肌质网上的细胞内Ca2 +释放通道的簇，并且高血压已被确定为钙释放单元功能缺陷的原因。我们的目的是确定耐力运动训练是否可以减轻高血压对自发性高血压大鼠左室心肌细胞钙释放单位成分和Ca2 +火花的有害影响。将雄性Wistar和自发性高血压大鼠（4个月大）分为4组：正常血压（NC）和高血压对照（HC），以及正常血压（NT）和高血压训练（HT）动物（每组7只大鼠）。将NC和HC大鼠接受低强度跑步机跑步方案（5天/周，1小时/天，0％坡度和最大跑步速度的50-60％）持续8周。与NC大鼠相比，HC中的ryanodine受体2型（RyR2）和FK506结合蛋白（FKBP12.6）的基因表达分别增加（270％）和减少（88％）。耐力运动训练通过减少RyR2（230％）和使FKBP12.6基因表达正常化（112％）来逆转这些变化。高血压还增加了Ca2 +火花的频率（HC = 7.61±0.26 vs NC = 4.79±0.19每100μm/ s）并降低了振幅（HC = 0.260±0.08 vs NC = 0.324±0.10ΔF/ F0）半最大振幅（HC = 1.05±0.08 vs NC = 1.26±0.01μm），总持续时间（HC = 11.51±0.12 vs NC = 14.97±0.24 ms），峰时间（HC = 4.84±0.06 vs NC = 6.31± 0.14 ms）和衰减时间常数（HC = 8.68±0.12 vs NC = 10.21±0.22 ms）。这些变化在HT大鼠中被部分逆转（Ca2 +火花频率= 6.26±0.19μm/ s，振幅= 0.282±0.10ΔF/ F0，半最大振幅时的全宽度= 1.14±0.01μm，总持续时间= 13.34±0.17 ms ，到达峰值的时间= 5.43±0.08 ms，衰减时间常数= 9.43±0.15 ms）。耐力运动训练减弱了高血压对左心室心肌细胞钙释放单位的有害作用。

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