表征的受体参与5-HT-induced激发狗窦的纵肌。
文章的细节
-
引用
复制到剪贴板 -
普林斯在北半球,Akkermans LM Lefebvre RA, Schuurkes农协
表征的受体参与5-HT-induced激发狗窦的纵肌。
Br J杂志。2001年11月,134 (6):1351 - 9。
- PubMed ID
-
11704657 (在PubMed]
- 文摘
-
1。我们旨在描述5 -受体参与5-HT-induced影响电体外诱导狗腔纵向肌肉的收缩。2。在L-NOARG(0.1毫米),电场刺激(EFS)诱导阿托品,tetrodotoxin-sensitive收缩。河豚毒素或阿托品离开任何兴奋剂测试无效。平均这些EFS-induced收缩增强5 - (0.3 microM),然而,明显的变化应对观察5。有选择性的非重要趋势5-HT3受体拮抗剂granisetron (1 microM)和二甲麦角新碱(1 microM;5-HT2,防止相互作用的5 - 5-HT1 5-ht5 5-HT6和5-HT7受体)增加5。选择性5-HT4受体拮抗剂GR 113808 (0.1 microM)显示抑制5-HT-induced增加的趋势。3所示。 Combination experiments with methysergide (1 microM), granisetron (1 microM) and GR 113808 (0.1 microM) revealed that the 5-HT (0.3 microM)-induced response consisted of (1) an excitatory component blocked by GR 113808, (2) excitatory and inhibitory components both blocked by methysergide. 4. The selective 5-HT4 receptor agonist prucalopride (0.3 microM) increased EFS-induced contractions, an effect prevented by GR 113808 (0.1 microM). 5. The increase of EFS-induced contractions by the preferential 5-HT2 receptor agonist alpha-Me-5-HT (0.3 microM) was antagonized by 5-HT2B receptor antagonists. 6. The 5-HT1/5-HT7 receptor agonist 5-carboxamidotryptamine (5-CT; 0.3 microM) inhibited EFS-induced contractions. This was prevented by methysergide (1 microM), the 5-HT7 receptor antagonist mesulergine (0.3 microM) and the selective 5-HT7 receptor antagonist SB-269970 (0.3 microM). 7. In the presence of GR 113808 (0.1 microM), alpha-Me-5-HT (1 microM) increased EFS-induced contractions. The 5-HT (0.3 microM)-induced inhibition of the stimulation by alpha-Me-5-HT was prevented by SB-269970 (0.3 microM). 8. In conclusion, dog antral longitudinal muscle is endowed with (1) excitatory neuronal 5-HT4 receptors and 5-HT2B receptors and (2) inhibitory smooth muscle 5-HT7 receptors.