| Autor: |
Sikorski, B. W., James, G. M., Glance, S. D., Hodgson, W. C., King, R. G. |
| Zdroj: |
Journal of Cardiovascular Pharmacology; September 1993, Vol. 22 Issue: 3 p423-430, 8p |
| Abstrakt: |
We investigated constrictor responses to 5-hy-droxytryptamine (5-HT) and l-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI, a 5-HT2/5-HT1creceptor agonist) of aortic rings from 2− and 6-week streptozotocin-diabetic and vehicle control rats. At 10 g resting tension, maximum responses and -log EC50values to 5-HT were significantly reduced in endothelium-intact and denuded aortas from 2− and 6-week diabetic rats relative to those from control rats (except for - log EC50of endothelium-intact rings from 6-week diabetic rats). Removal of endothelium from aortas of 2− and 6-week diabetic and control rats caused significant increases both in -log EC50values and in maximum responses to 5-HT. DOI caused marked contraction of endothelium-denuded aortas from control rats, but not of endothelium-intact aortas from control rats or aortas (either with or without endothelium) from diabetic rats. The nitric oxide (NO) synthase inhibitor N-nitro-L-arginine (NOLA) significantly potentiated constrictor responses to 5-HT in endothelium-intact aortas from control and diabetic rats. NOLA significantly potentiated constrictor responses to DOI in endothelium-intact aortas from control rats, but not in endothelium-intact aortas from diabetic rats. These results suggest that for aortas from 2− and 6-week diabetic rats, the diminished responses to 5-HT and DOI may be a result of reductions in 5-HT2-receptor-mediated responses of smooth muscle. The results also suggest that 5-HT and DOI can stimulate NO release from endothelial cells. |
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