Iemitsu Motoyuki, Maeda Seiji, Otsuki Takeshi, Goto Katsutoshi, Miyauchi Takashi
Center for Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan.
Exp Biol Med (Maywood). 2006 Jun;231(6):871-5.
Endothelin (ET)-1 is produced by endothelial cells and cardiac myocytes. ET-1 has positive inotropic and chronotropic effects on the heart and causes myocardial cell hypertrophy. Exercise training induces a physiologic cardiac hypertrophy. To study whether myocardial ET-1 is involved in the formation of exercise training-induced cardiac hypertrophy, we investigated time-course alterations of myocardial ET-1 gene expression and ET-1 peptide level in the heart of rats during a formative process of exercise training-induced cardiac hypertrophy. We used the hearts of rats that had been exercise-trained for 4 weeks (4WT) or 8 weeks (8WT) and sedentary control rats for 4 weeks (4WC) or 8 weeks (8WC). Exercise-trained rats performed treadmill running for 5 days/week (60 mins/day). Left ventricular mass index and wall thickness and stroke volume index, measured using echocardiography, in the 8WT group were significantly greater than in the 8WC group, although there were no differences between the 4WC and 4WT groups in these parameters. These results indicated that the 8WT rats developed physiologic cardiac hypertrophy, whereas the 4WT rats did not yet have cardiac hypertrophy. Myocardial ET-1 gene expression and tissue ET-1 concentration in the heart were significantly higher in the 8WT group than in the 8WC group, whereas these values did not differ between the 4WC and 4WT groups. The present study suggests that an alternation of myocardial ET-1 production corresponds with the formation of exercise training-induced cardiac hypertrophy. Therefore, the exercise training-induced change in myocardial ET-1 production may participate in a mechanism of exercise training-induced cardiac adaptation (e.g., cardiac hypertrophy).
内皮素（ET）-1由内皮细胞和心肌细胞产生。ET-1对心脏具有正性变力和变时作用，并可导致心肌细胞肥大。运动训练可诱导生理性心脏肥大。为研究心肌ET-1是否参与运动训练诱导的心脏肥大的形成，我们调查了运动训练诱导的心脏肥大形成过程中大鼠心脏中心肌ET-1基因表达和ET-1肽水平的时间进程变化。我们使用了运动训练4周（4WT）或8周（8WT）的大鼠心脏以及久坐对照大鼠4周（4WC）或8周（8WC）的心脏。运动训练的大鼠每周进行5天跑步机跑步（每天60分钟）。尽管4WC组和4WT组在这些参数上没有差异，但8WT组使用超声心动图测量的左心室质量指数、壁厚度和每搏输出量指数显著高于8WC组。这些结果表明，8WT大鼠发生了生理性心脏肥大，而4WT大鼠尚未出现心脏肥大。8WT组心脏中的心肌ET-1基因表达和组织ET-1浓度显著高于8WC组，而4WC组和4WT组之间这些值没有差异。本研究表明，心肌ET-1产生的改变与运动训练诱导的心脏肥大的形成相对应。因此，运动训练诱导的心肌ET-1产生变化可能参与运动训练诱导的心脏适应机制（如心脏肥大）。
