The role of serotonin in the preeclampsia-eclampsia syndrome

The cause of preeclampsia, a syndrome unique to human pregnancy, is unknown. There is presently no effective pharmacologic therapy once the symptoms have appeared. Only delivery is curative. Preeclampsia likely has multiple etiologies, each of which activates a common pathway, culminating in diffuse endothelial damage, vasospasm, and hypertension. Current investigation suggests that serotonin has a pivotal role in the genesis of preeclamptic hypertension. The evidence, as obtained from human and animal study, is reviewed in this article, and areas in need of further study are highlighted. A modified series of Koch's postulates is employed for a framework. Serotonin is the agent but does not directly cause the hypertension. Rather, it is suggested that in a milieu characterized by a reduction in endothelial-derived relaxing factor and prostacyclin, serotonin augments the smooth muscle response to normally occurring concentrations of endogenous vasopressors. It is delivered to the site of action (the microvasculature) by the platelet, whose aggregation is encouraged by dysfunctional endothelium. Either inhibition of the delivery mechanism by a low, daily dose of aspirin, or inhibition of the peripheral serotonin type 2 (5HT2) receptor, effectively controls the hypertension.