ангиотензин II 通过降低TRPV4通道的调节,诱导内皮功能障碍和血管重塑
Narendra Babu Kondapalli1, Venkatesh Katari1, Kesha Dalal1
1Department of Physiology and Pharmacology, College of Medicine and Life Sciences, The University of Toledo, Toledo, OH 43614, USA.
Journal of molecular and cellular cardiology plus
|February 9, 2024
概括
ангиотензин II 降低内皮细胞中TRPV4通道的调节,损害氧化的产生,并导致血管改造和高血压.
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞功能 内皮细胞功能
- 高血压研究 高血压研究
背景情况:
- ангиотензин II (Ang II) 是一种已知的血管收缩剂,与高血压有关.
- 对Ang II在内皮功能中的作用及其与TRPV4通道的相互作用尚不清楚.
- 暂时受体潜在瓦尼洛伊德4 (TRPV4) 在内皮细胞中通过氧化 (NO) 调解血管扩张.
研究的目的:
- 研究Ang II对人类内皮细胞 (EC) 中TRPV4表达和功能的影响.
- 在体外和体内探索Ang II对TRPV4/eNOS通路的影响.
- 为了确定Ang II诱导的内皮功能障碍是否有助于高血压中的血管重塑.
主要方法:
- 用Ang II治疗的人体内皮细胞培养.
- 测量TRPV4蛋白和mRNA表达,Ca2+流入和eNOS酸化.
- 对NO生产的评估.
- 在体内研究中,使用注射Ang II的小鼠来评估TRPV4/p-eNOS表达和中腔动脉中的血管重塑.
主要成果:
- 安格II治疗降低了TRPV4蛋白表达的调节,并减少了TRPV4介导的人体EC中的Ca2+流入.
- 在Ang II治疗后,TRPV4诱导的氧化生产和eNOS酸化显著下降.
- 在体内,Ang II输液降低了TRPV4和酸化eNOS在内皮中的表达,并诱导了血管重塑.
结论:
- ангиотензин II 通过降低TRPV4/eNOS通路的调节,损害内皮功能.
- 这种下调有助于内皮功能障碍和血管重塑.
- 这些发现表明一种新的机制,Ang II可以促进高血压,独立于其直接的血管收缩作用.
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