Significance of defective endothelial signal transduction in impaired endothelium-dependent relaxation in atherosclerosis.
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.
Research Institute of Angiocardiology, Kyushu University School of Medicine, Fukuoka, Japan.
H
H
Shimokawa
R
R
Nakaike
A
A
Takeshita
D000818:Animals; D003324:Coronary Artery Disease / Q000503:physiopathology*; D003331:Coronary Vessels / Q000378:metabolism; D004730:Endothelium, Vascular / Q000503:physiopathology*; D019204:GTP-Binding Proteins / Q000378:metabolism; D006801:Humans; D008297:Male; D037342:Pertussis Toxin; D015398:Signal Transduction; D013552:Swine; D014664:Vasodilation; D010566:Virulence Factors, Bordetella / Q000494:pharmacology
D010566:Virulence Factors, Bordetella; D037342:Pertussis Toxin; D019204:GTP-Binding Proteins