[Participate of nitric oxide participate in hypoxic regulation of cerebrovascular tension].
Making use of nitric oxide synthesase (NOS) inhibitor Nw-nitric-oxide-L-arginine (L-NNA), the effect of NO and the pressence of endothelial cell on hypoxia-induced vascular dilatation was studied with new-born calve basilar artery. The experimental results show that L-NNA can attenuate the hypoxia-induced vascular dilatation, but the magnitude of attenuation is smaller than that of constriction caused by L-NNA on normoxic calve basilar artery. Under hypoxia, the vascular dilatation of endothelial cell denuded artery is smaller than that of endothelial cell intact artery; the difference between them is approximate by the same as the change caused by L-NNA on endothelial call intact artery. After destroying the endothelial cell, L-NNA has no obvious effect on the vascular tension. These results suggest that NO and endothelial cell are involved in hypoxia-induced vascular dilaxation.
Gu
Z Z
ZZ
Shanghai Institute of Physiology, Chinese Academy of Sciences.
Mei
X J
XJ
Zhong
K S
KS
Lu
M
M
D000818:Animals; D000831:Animals, Newborn; D001488:Basilar Artery / Q000473:pathology / Q000503:physiopathology*; D002417:Cattle; D004730:Endothelium, Vascular / Q000502:physiology*; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D014664:Vasodilation / Q000502:physiology*
D019335:Nitroarginine; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase