[The role of nitric oxide in the development of reactive hyperemia in the coronary bed].
De-endothelialization of the coronary vessels induced a 3-4-fold decrease in the level of hyperemia in anesthetised dogs. Infusion of L-arginine augmented the reactive hyperemia and the endothelium-dependent relaxation in response to acetylcholine administration. The reactive hyperemia seems to be wholly depending on the endothelium, being conditioned by the effect of endothelium-derived nitric oxide.
Sagach
V F
VF
Tkachenko
M N
MN
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D004285:Dogs; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D005260:Female; D006940:Hyperemia / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D009569:Nitric Oxide / Q000502:physiology*; D019335:Nitroarginine; D010208:Papaverine / Q000494:pharmacology; D012503:Saponins / Q000494:pharmacology
D012503:Saponins; D019335:Nitroarginine; D009569:Nitric Oxide; D001120:Arginine; D010208:Papaverine; D000109:Acetylcholine