Abstract
Background. We investigated the effect of nitric oxide and prostacyclin, which are endothelium-derived vasodilators, on serotonin (5-HT)-induced vasocontraction, and 5-HT1-serotoninergic receptor mediated relaxation in the human umbilical artery. Methods. Serotonin-stimulated vasocontraction was measured in umbilical artery segments treated with and without 1) L-arginine (10−4 M∼10−2 M), a precursor of nitric oxide synthesis: 2) methylene blue (10−5 and L-NG-monomethyl arginine (LNMA, 2×10−4 M), which are specific inhibitors of nitric oxide action and nitric oxide synthesis, respectively; and 3) tranylcypromine (2X 10−7 M. 2×10−5 M), an inhibitor of prostacyclin synthesis. 4) Vessels were pretreated with M1. an inhibitor of 5-HT2 serotoninegic receptors, and then prostaglandin F2 α (9.0×10−7 M). Finally, we measured the 5-HT1 receptor-mediated relaxation induced by 5-HT.
Results. Treatment with L-arginine significantly inhibits 5-HT-induced contraction in a dose-dependent manner. Treatment with methylene blue and LNMA significantly potentiated 5-HT-induced contraction. Tranylcypromine caused no significant changes in 5-HT-induced vasocontraction. 5-HT1 serotoninetic receptor-mediated relaxation was found at higher concentrations of 5-HT (greater than 4.94X 10−5 M).
Conclusions. Our results suggest that nitric oxide may exert a strong relaxant effect on 5-HT-induced vasocontraction compared with prostacyclin in human umbilical artery.