Serotonin-Induced Vasoconstriction in the Perfused Canine Femoral Artery Can Be Blocked in Vivo by Ketanserin

Abstract

Serotonin, applied to helical strips of larger vessels such as coronary arteries, acts as a potent vasoconstrictor in vitro. In contrast, in vivo serotonin causes a remarkable decrease in total peripheral resistance. To differentiate the influence of serotonin on resistances of large and small vessels, experiments were done in nine anesthetized dogs. The left iliacal artery was cannulated and blood flow into the femoral artery was kept constant by a roller pump. Mean proximal femoral artery pressure and mean dorsal pedal artery pressure were measured. Pressure gradient (delta P), resistances between proximal femoral artery and dorsal pedal artery (R1), dorsal pedal artery and right atrium (R2), as well as total peripheral resistance were calculated during systemic infusion of 50 micrograms/kg X min serotonin. Serotonin caused a significant increase in delta P and R1 and a decrease in R2 and total peripheral resistance. Pretreatment with 100 micrograms/kg ketanserin abolished the significant change in delta P and R1, whereas the decrease in R2 and total peripheral resistance was not affected. Additional experiments with prazosin showed that alpha-receptors are obviously not involved in the responses observed. Isosorbide dinitrate, which was infused to differentiate passive and active narrowing of vessels, showed a serotoninlike decrease in mean dorsal pedal artery pressure but no change in either delta P or R1. The 5--HT2-serotonergic antagonist ketanserin blocked serotonin-induced constriction of large vessels in vivo but not the dilation of small arteries.