当NOS被抑制时,TRPA1通道在年轻成年人中在高温运动期间调节皮肤血管扩张
Rei Hattori1, Masanobu Kajiki1, Tomomi Fujimoto2
1Institute of Health and Sport Sciences, University of Tsukuba, Ibaraki, Japan.
概括
暂时受体潜在的安基林1 (TRPA1) 通道在运动中帮助皮肤血液流动,但只有当氧化合成酶 (NOS) 被阻塞时. 当NOS受到损害时,TRPA1充当血管扩张的备用系统.
科学领域:
- 身体生理学 身体生理学
- 热调节 热调节 热调节
- 心血管科学 心血管科学
背景情况:
- 氧化合成酶 (NOS) 在运动和暴露于热量期间对皮肤血管扩张至关重要.
- 此前发现过渡受体潜在安基林1 (TRPA1) 通道通过静止状态的NOS-依赖通路调解血管扩张.
- TRPA1在运动热应激联合过程中的血管扩张中的作用尚不清楚.
研究的目的:
- 通过NOS依赖的机制,研究TRPA1通道激活通过NOS依赖的机制在高温运动中促进皮肤血管扩张的假设.
- 为了确定TRPA1通道是否在运动热应激期间在维持皮肤血流方面发挥作用,特别是当NOS受到抑制时.
主要方法:
- 一项替代研究验证了使用TRPA1激动剂ASP7663.3的TRPA1抗剂HC030031的疗效.
- 参与者 (n=12) 在热 (35°C) 中进行了两次骑自行车比赛.
- 在用DMSO (对照剂),HC030031 (TRPA1抗剂),l-NAME (NOS抑制剂) 或组合HC030031 + l-NAME治疗前臂皮肤后,测量了皮肤血管导电性 (CVC).
主要成果:
- 与对照人群相比,单独的TRPA1抗剂HC030031在高温运动期间对CVC没有影响.
- 通过l-NAME显著降低NOS抑制的CVC.
- 结合l-NAME和HC030031治疗导致CVC的减少比单独使用l-NAME更大,这表明TRPA1在抑制NOS时的作用.
结论:
- 在运动热应激过程中,TRPA1通道调解皮肤血管扩张,但主要是当氧化合成酶 (NOS) 途径受到抑制时.
- 在运动-热应激条件下,TRPA1通道可能充当补偿或"备份"系统,以维持皮肤血液流动,当NOS-依赖的血管扩张受到损害时.
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