Effect of hydroxocobalamin on vasodilatations to nitrergic transmitter, nitric oxide and endothelium-derived relaxing factor in guinea-pig basilar artery.
In endothelium-denuded guinea-pig isolated basilar artery preparations, hydroxocobalamin (30, 100 and 300 microM) concentration-dependently inhibited the vasodilator responses to exogenous nitric oxide (NO), whereas the vasodilator responses to nitrergic nerve stimulation were slightly reduced by high (100 and 300 microM) but not by the low (30 microM) concentration of hydroxocobalamin. Vasodilatation in response to sodium nitroprusside (10-100 nM) was totally abolished by 300 microM hydroxocobalamin. In endothelium-intact preparations, vasodilator responses to acetylcholine (0.3-3 microM) were significantly reduced or abolished by hydroxocobalamin (30-300 microM). The mean reduction by hydroxocobalamin of relaxations to acetylcholine was significantly greater than that of the equivalent response evoked by nitrergic nerve stimulation. The findings suggest that the nitrergic transmitter in the guinea-pig basilar artery may be quantitatively less susceptible than the endothelium-derived relaxing factor to the NO scavenger hydroxocobalamin.
Jiang
F
F
Department of Medical Laboratory Science, Royal Melbourne Institute of Technology, Vic., Australia.
Li
C G
CG
Rand
M J
MJ
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001488:Basilar Artery / Q000187:drug effects*; D015237:Dinoprost / Q000494:pharmacology; D005260:Female; D006168:Guinea Pigs; D006397:Hematinics / Q000494:pharmacology*; D006879:Hydroxocobalamin / Q000494:pharmacology*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009569:Nitric Oxide / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects*
D006397:Hematinics; D009599:Nitroprusside; D009569:Nitric Oxide; D015237:Dinoprost; D000109:Acetylcholine; D006879:Hydroxocobalamin