Serotonin-Induced Vasoconstriction in Human Placental Chorionic Veins: Interaction with Prostaglandin F₂_α

Abstract

In vitro experiments using isolated rings and perfused segments of humanchorionic veins, were designed to determine the effects of serotonin and their interaction with PGF_2Α on vascular tension and perfusion pressure. These vessels responded vigorously with high sensitivity to the vasoconstrictor effects of serotonin in both experimental designs. Administration of PGF_2Α also led to constriction of the veins, but this autacoid is at least 100 times less potent than serotonin. When adding PGF_2Α previously to serotonin to the bathing fluid or to the perfusate, the serotonin response was significantly potentiated, increasing the maximal contractile response in 116 ± 12 % and the perfusion pressure in 180 ± 25%. Both autacoids probably operate in this vascular bed interacting with each other and playing an important role in the regulation of placental blood flow in vivo

Differential Serotonin Uptake Mechanisms at the Human Maternal–Fetal Interface

“…It modulates a number of cellular processes in placental cells, including proliferation, cell viability, cell cycle progression, apoptosis, and estrogen production [5][6][7][8][9]. As a potent vasoactive autacoid, 5-HT also influences the utero-placental and feto-placental blood flow [10,11]. Early in pregnancy, the placenta supplies the developing fetus with maternal and/or placenta-derived 5-HT, which is required for proper fetal (neuro)development [12][13][14].…”

The platelet serotonergic system and the search for new biomarkers and therapeutic options for diverse diseases

“…According to multiple reports on women with preeclampsia, the existence of hyperserotonemia during preeclampsia exacerbates several pathological processes, such as endothelial cell damage, platelet aggregation, the development of turbulence in blood flow, and microvascular damage in the placenta, all leading to more abundant inflammation [24,123]. Damage to endothelial cells promotes platelet aggregation and as a consequence the release of 5-HT, which induces vasoconstriction mediated by 5-HT2 receptors in smooth muscle tissue and the uterine artery [25,124].…”