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Smoking, endothelial function, and Rho-kinase in humans
Kensuke Noma1, Chikara Goto, Kenji Nishioka
1Department of Cardiovascular Physiology and Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Arteriosclerosis, Thrombosis, and Vascular Biology
|October 8, 2005
Summary
Smoking impairs blood vessel function and increases Rho-kinase activity in vascular smooth muscle cells (VSMCs). This study found a direct link between smoking-induced endothelial dysfunction and Rho-kinase activation in young men.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Vascular Biology
Background:
- Smoking is a major risk factor for cardiovascular disease.
- It is known to cause endothelial dysfunction and activate Rho-kinase in vascular smooth muscle cells (VSMCs).
Purpose of the Study:
- To investigate the relationship between endothelial function and Rho-kinase activity in forearm VSMCs of healthy young men.
Main Methods:
- Forearm blood flow (FBF) responses to acetylcholine (ACh), fasudil (a Rho-kinase inhibitor), and sodium nitroprusside (SNP) were measured in male smokers and nonsmokers using strain-gauge plethysmography.
Main Results:
- Smokers exhibited a reduced vasodilatory response to ACh compared to nonsmokers.
- The vasodilatory effect of fasudil was significantly greater in smokers, indicating increased Rho-kinase activity.
- Fasudil coinfusion improved the ACh response in smokers, suggesting a link between Rho-kinase and endothelial dysfunction.
Conclusions:
- Smoking contributes to both endothelial dysfunction and Rho-kinase activation in forearm circulation.
- A significant correlation exists between endothelial function and Rho-kinase activity in VSMCs in the context of smoking.