The significance of the defective endothelial signal transduction in the impaired endothelium-dependent relaxations in atherosclerosis and related conditions was examined. Pertussis toxin-sensitive endothelium-dependent relaxations were prominently impaired in experimental atherosclerosis in pigs. The expression of endothelial Gi protein was reduced in atherosclerosis and related conditions in human coronary arteries. Thus, the dysfunction of pertussis toxin-sensitive G protein (Gi protein) may contribute to the impairment of the endothelium-dependent relaxations in atherosclerosis.
- Endothelium-dependent relaxation
- Endothelium-derived relaxing factor
- Gi protein
- Nitric oxide
ASJC Scopus subject areas
- Geriatrics and Gerontology