Pathophysiology of preeclampsia and the role of serotonin

Hypertensive disorders constitute the most common medical complications of pregnancy. In normal pregnancy, impressive physiological changes take place in the maternal cardiovascular system. Morphological changes are the resul t of invasion of migratory trophoblast cells into the walls of the spiral a rteries. After destruction of elastic, muscular and neural tissue in the me dia, the trophoblast cells get incorporated into the vessel wall and the en dothelial lining of the spiral arteries is restored. The physiological chan ges create a low-resistance, low-pressure, high-flow system with the absenc e of maternal vasomotor control. Biochemical adaptations in maternal vascul ature include changes in the prostaglandin system, the renin-angiotensin-al dosteron system and the kallikrein-kinin system. In preeclampsia, physiological changes in the spiral arteries are confined to the decidual portion of the arteries. Myometrial segments remain anatomi cally intact and fail to dilate. In addition, the adrenergic nerve supply i s left intact. The cause of this impaired endovascular trophoblast invasion is not yet elucidated. But in combination with the imbalance between vasod ilator and vasoconstrictor eicosanoids, it gives rise to reduced perfusion of the intervillous space. in the absence of an adequate production of anti aggregatory prostacyclin (PGI(2)), nitric oxide, or both, surface-mediated platelet activation is supposed to occur on the surface of the spiral arter ies. Because platelets are the principal source of circulating serotonin, t he increased platelet aggregation in preeclampsia causes an increase in ser otonin levels. Interaction of serotonin with serotonin(1)- or serotonin(2)- receptors depends on the state of the endovascular trophoblast or endotheli um in the spiral arteries and has opposite effects with regard to vasodilat ing and vasoconstrictive influences. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.