Datté Jacques Y, Yapo Paul A, Offoumou Michel A
Laboratoire de Nutrition et Pharmacologie , UFR-Biosciences, Cocody Université, Abidjan, 20 BP 947 Abidjan 20, République de Côte d'Ivoire.
Pharmacol Rep. 2005 Jan-Feb;57(1):113-20.
The aim of the present study was to investigate a nitric oxide (NO) involvement in the mediation of a 5-HT-induced vasoconstriction response in the rat portal vein in vitro. Isolated rat portal vein segments were placed in organ baths for isometric force measurement. 5-HT (3 x 10(-8) M-3 x 10(-4) contracted portal vein preparations (EC50 = 7 x 10(-7) M) in a concentration-dependent manner. The vasoconstriction induced by 5-HT was significantly increased in endothelium-denuded vessels. Pretreatment with Nomega-nitro-L-arginine methyl ester (L-NAME 100 microM) enhanced the contractive response to 5-HT either in intact or endothelium-denuded vessels. However, ketanserin (0.1 microM) abolished 5-HT-induced vasoconstrictions (EC50 = 4.6 x 10(-8) M). Furthermore, a non-selective 5-HT(1B/D) receptor agonist, sumatriptan (1 x 10(-10) M-1 x 10(-5) M), induced a reduction of spontaneous rhythmic contractions also in endothelium-intact vessels. However, 5-HT- induced vasoconstriction was unaffected by propranolol (10 microM). The data support the hypothesis of the existence of serotonergic innervations modulating the contractility of vascular smooth muscle. These findings are consistent with the hypothesis that the vasoconstrictor activity of 5-HT in smooth muscle was mediated by activation of 5-HT(1B/D) and 5-HT(2B) receptor subtypes involving the endothelium-dependent mechanism.
本研究的目的是调查一氧化氮（NO）在体外介导大鼠门静脉5-羟色胺（5-HT）诱导的血管收缩反应中的作用。将分离的大鼠门静脉段置于器官浴槽中进行等长力测量。5-HT（3×10⁻⁸ M - 3×10⁻⁴ M）以浓度依赖性方式使门静脉制剂收缩（EC50 = 7×10⁻⁷ M）。5-HT诱导的血管收缩在去内皮血管中显著增强。用Nω-硝基-L-精氨酸甲酯（L-NAME，100 μM）预处理可增强完整或去内皮血管对5-HT的收缩反应。然而，酮色林（0.1 μM）可消除5-HT诱导的血管收缩（EC50 = 4.6×10⁻⁸ M）。此外，一种非选择性5-HT（1B/D）受体激动剂舒马曲坦（1×10⁻¹⁰ M - 1×10⁻⁵ M）也可使内皮完整的血管中的自发节律性收缩减少。然而，5-HT诱导的血管收缩不受普萘洛尔（10 μM）的影响。这些数据支持存在调节血管平滑肌收缩性的5-羟色胺能神经支配这一假说。这些发现与以下假说一致，即5-HT在平滑肌中的血管收缩活性是通过激活5-HT（1B/D）和5-HT（2B）受体亚型介导的，且涉及内皮依赖性机制。
