Abstract
In endothelium-denuded guinea-pig isolated basilar artery preparations, hydroxocobalamin (30, 100 and 300 μM) 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 μM) but not by the low (30 μM) concentration of hydroxocobalamin. Vasodilatation in response to sodium nitroprusside (10-100 nM) was totally abolished by 300 μM hydroxocobalamin. In endothelium-intact preparations, vasodilator responses to acetylcholine (0.3-3 μM) were significantly reduced or abolished by hydroxocobalamin (30-300 μM) Tile 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.
| Original language | English |
|---|---|
| Pages (from-to) | 181-186 |
| Number of pages | 6 |
| Journal | European Journal of Pharmacology |
| Volume | 340 |
| Issue number | 2-3 |
| DOIs | |
| Publication status | Published - 11 Dec 1997 |
| Externally published | Yes |
Keywords
- Basilor artery
- EDRF (endothelium-derived relaxing factor)
- Endothelium-denuded
- Guinea-pig
- Hydroxocobalamin
- Niric oxide (NO)
- Nitrergic transmitter
- Vasodilatation