ABSTRACT
PURPOSE: The aim of the present study was to investigate a nitric oxide (NO) involvement in the mediation of a 5-HT-induced vasoconstrictions response in the rat portal vein in vitro. MATERIAL AND METHODS: Isolated rat portal vein preparations obtained after dissection were placed in organ baths for isometric force measurement via a strain gauge. RESULTS: 5-hydroxytryptamine (5-HT) in concentrations ranging from 3x10(-8) M to 3x10(-4) M contracted portal vein preparations (EC50= 7x10(-7) M) in a concentration dependent manner. The vasoconstrictions induced by 5-HT was significantly increased in endothelium-denuded vessels. Pre-treatment with N(omega)-nitro-L-arginine methyl Ester (L-NAME 100 microM) enhanced the contractive response to 5-HT either in intact- or denuded endothelium vessels. Whereas, ketanserin (0.1 microM) abolished 5-HT-induced vasoconstrictions (EC50= 4.6x10(-8) M). Furthermore, a non-selective 5-HT receptors agonist, sumatriptan, (1x10(-10 )M - 1x10(-5) M) induced a reduction of spontaneous rhythmic contractions either in endothelium-intact or in endothelium -denuded vessels. However, 5-HT-induced vasoconstriction was unaffected by propranolol (10 microM). CONCLUSIONS: These findings are consistent with the hypothesis that the vasoconstrictor activity of 5-HT in vascular smooth muscle was mediated by activation of 5-HT1B/D and 5-HT2B receptors subtypes involving the endothelium (NO) dependent mechanism.
