Relaxant effect of nitric oxide and prostacyclin on serotonin‐induced vasocontraction of human umbilical artery

Background. We investigated the effect of nitric oxide and prostacyclin, which are endothelium‐derived vasodilators, on serotonin (5‐HT)‐induced vasocontraction, and 5‐HT 1 ‐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‐N G ‐monomethyl arginine (LNMA, 2×10 −4 M), which are specific inhibitors of nitric oxide action and nitric oxide synthesis, respectively; and 3) tranylcypromine (2× 10 −7 M. 2×10 −5 M), an inhibitor of prostacyclin synthesis. 4) Vessels were pretreated with M 1 . an inhibitor of 5‐HT 2 serotoninegic receptors, and then prostaglandin F 2 α (9.0×10 −7 M). Finally, we measured the 5‐HT 1 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‐HT 1 serotoninetic receptor‐mediated relaxation was found at higher concentrations of 5‐HT (greater than 4.94× 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.