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内皮衍生的高极化因子决定了休息和刺激的前臂血管扩展体调在健康和疾病中
Muhiddin A Ozkor1, Jonathan R Murrow, Ayaz M Rahman
1Emory Clinical Cardiovascular Research Institute, Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA, USA.
Circulation
|May 11, 2011
概括
内皮衍生的高极化因子 (EDHFs) 通过激活K+(Ca) 通道和释放环氧乙酸,有助于血管度. EDHFs有助于维持血液流动,特别是当氧化减少时,如高胆固醇血症中所见.
科学领域:
- 心血管生理学心血管生理学
- 内皮细胞功能 内皮细胞功能
- 血管生物学 血管生物学
背景情况:
- 内皮衍生的高极化因子 (EDHF) 在调节血管度方面发挥作用.
- 像四乙氨化物 (TEA) 和可纳醇这样的抑制剂被用于研究EDHF通路.
- 该研究调查了EDHF对休息和刺激血管扩张在健康和疾病中的贡献.
研究的目的:
- 评估EDHFs在休息和激动剂刺激的血管扩展体度中的作用.
- 为了确定EDHF是否可以弥补氧化生物利用率的降低.
- 研究EDHF作用的机制,包括K+(Ca) 通道激活和环氧乙酸合成.
主要方法:
- 在103名健康和71名非高血压受试者中,使用静脉闭塞整体图测量了前臂血流 (FBF).
- 进行了N(G) - 单甲基-l-氨酸 (L-NMMA),TEA和可纳的静脉内输注.
- 分析了这些药物的对静止FBF和由布拉迪基宁和乙胆诱导的血管扩张的影响.
主要成果:
- 在所有受试者中,L-NMMA和TEA降低了休息FBF,在健康受试者中,L-NMMA反应更大,TEA反应更低.
- 可纳降低了静止FBF,其与TEA的组合进一步降低了FBF,表明细胞染色体P450代谢产物和其他EDHF的参与.
- L-NMMA和TEA都减弱了布拉迪基宁介导的血管扩张;TEA仅在高胆固醇血症中影响了乙胆介导的血管扩张.
结论:
- 通过TEA可抑制的K+(Ca) 通道和氧化,EDHFs有助于休息的微血管音调.
- K+(Ca) 通道的激活部分由环氧酸介导,但其他EDHF机制也存在.
- 在高胆固醇血症中,EDHF活性弥补了氧化的减少,在休息和激动剂刺激期间保持血管扩张.
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