Involvement of nitric oxide in fading of 5-hydroxytryptamine-induced vasocontraction in rat isolated vena portae smooth muscle.

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 concentra-tions ranging from 3x10-8 M to 3x10-4 M contracted portal vein preparations (EC50 = 7x10-7 M) in a concen-tration dependent manner. The vasoconstrictions induced by 5-HT was significantly increased in endot-helium-denuded vessels. Pre-treatment with Nw-nitro-L-arginine methyl Ester (L-NAME 100 µM) enhanced the contractive response to 5-HT either in intact- or denuded endothelium vessels. Whereas, ketanserin (0.1 µM) abolished 5-HT-induced vasoconstrictions (EC50 = 4.6x10-8 M). Furthermore, a non-selective 5-HT1B/D- receptors agonist, sumatriptan, (1x10-10 M-1x10-5 M) induced a reduction of spontaneous rhyth-mic contractions either in endothelium-intact or in endothelium –denuded vessels. However, 5-HT-induced vasoconstriction was unaffected by propra-nolol (10 µM). Conclusions: These findings are con-sistent with the hypothesis that the vasoconstrictor activity of 5-HT in vascular smooth muscle was medi-ated by activation of 5-HT1B/D and 5-HT2B receptors subtypes involving the endothelium (NO) dependent mechanism