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

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.