Exercise and regulation of circulatory system by endothelium-derived vasoactive substances

本研究旨在探讨内皮源性血管活性物质（内皮素-1（ET-1）和一氧化氮（NO））是否参与运动时的循环调节。本研究的成果如下。首先，我们用ET-1拮抗剂证明了ET-1介导的血管收缩作用参与了运动引起的组织血流量的再分配，即运动时内脏器官血流量的减少和活动肌肉血流量的增加。此外，它揭示了在运动期间肾脏中ET-1产生的增加有助于肾脏中NO产生的减少。因此，在内部器官的血管中，增加的ET-1似乎有助于运动引起的血流再分配，其直接作用和抑制血管舒张作用的NO。第二，我们证明了运动训练引起的ET-1生产减少和NO生产增加在健康的年轻人和老年人。此外，我们发现，内皮型一氧化氮合酶（eNOS）的基因和蛋白表达的大鼠主动脉随着年龄的增长而减少，而表达的运动训练增加。第三，我们研究了大动脉的扩张性和顺应性，这可能会受到内皮源性血管活性物质的影响，是否会改变急性运动和短期运动训练的人。我们证明了在急性运动期间大动脉的扩张性升高，并且短时间的运动训练导致休息时和运动期间全身动脉顺应性增加。我们提出一种可能性，运动引起的内皮功能的改变可能与大动脉扩张性和顺应性的快速增加。

The purpose of the present study was to investigate whether the endothelium-derived vasoactive substances (endothelin-1 [ET-1], a potent vasoconstrictor peptide, and nitric oxide [NO], a potent vasodilator substance) participate in the circulatory regulation during exercise. The products of this study are follows. First, by using ET-1 antagonist, we demonstrated that the ET-1-mediated vasoconstriction participates in the exercise-induced redistribution of tissue blood flow, I.e. the decrease of blood flow internal organs and the increase of blood flow active muscles during exercise. Furthermore, it was revealed that an increase of ET-1 production in the kidney during exercise contributes to a decrease of NO production in the kidney. Therefore, in the blood vessels of the internal organs, the increased ET-1 appears to contribute to the exercise-induced redistribution of blood flow by its direct action and by inhibiting the vasodilative action of NO. Second, we demonstrated that the exercise training caused a decrease in ET-1 production and an increase in NO production in both healthy young and older humans. Furthermore, we showed that the gene and protein expression of endothelial NO synthase (eNOS) in the aorta of rat is decreased by aging, and that the expression is increased by exercise training. Third, we examined whether the distensibility and compliance of large arteries, which may be affected by the endothelium-derived vasoactive substances, are altered with an acute exercise and the exercise training of short-duration in humans. We demonstrated that the distensibility of large arteries is elevated during an acute exercise, and that the exercise training of short-duration causes an increase of systemic arterial compliance at rest and during exercise. We propose a possibility that the exercise-induced alteration of endothelial functions might be related to the rapid increase of large arterial distensibility and compliance.