Preeclampsia is a human pregnancy-specific disorder, which refers to the new onset of hypertension (140/90 mmHg) and proteinuria after 20 wk of gestation in previously normotensive, nonproteinuric women. The incidence of preeclampsia is between 3% and10% of pregnancies, and there is no evidence that this has changed appreciably during the last century. Despite being one of the leading causes of maternal death and a major contributor to maternal and perinatalmorbidity, the etiology and pathogenesis of preeclampsia have not been fully defined.Preeclampsia occurs only in the presence of the placenta or a hydatidiform mole and remits dramatically postpartum after the delivery of the placenta. The pathogenesis of preeclampsia may involve abnormal cytotrophoblast invasion of spiral arterioles, decreased uteroplacental hypoperfusion, an imbalance between increased synthesis of thromboxane and decreased production of prostaglandin 12, increased oxidative stress, disordered endothelin metabolism, or endothelial dysfunction.Corticotrophin-releasing hormone (CRH) is a 41 amino acid peptide hormone first identified in the hypothalamus of mammals, where it acts as the main physiological regulator of corticotrophin (ACTH) secretion from corticotropes of the anterior pituitary, and plays a critical role in co-ordination of the neuroendocrineresponse to stress. CRH is also produced in a variety of tissues outside the CNS, including the gut, ovary and testis. During human pregnancy, the placenta and fetal membranes produce large amounts of CRH.It is generally believed that CRH is a potent vasorelaxant. Addition to control of cortisol levels in the body, CRH may play a direct role in regulation of blood pressure by endothelium-dependent and endothelium-independent mechanisms of vasorelaxation. Recently, some in vitro tests have also shown that CRH can significantly stimulated human trophoblast proliferation in first-trimester, and may plays a role in trophoblast invasion.It has thus been postulated that CRH participates in the development of preeclampsia. Although there have been already several studies describing a higher CRH level in serum from patients with preeclampsia than from normal pregnancies, few studies about placenta. The objectives of our investigation were to detect CRH in serum and placenta of preeclampsia.The subjects are 36 patients who were diagnosed with preeclampsia during the period from January to December of 2005, and underwent selective cesarean section. The ages of these subjects ranged 21 years to 39 years with a median of 29.5 years and the gestational ages at delivery 28 weeks to 41 weeks with a median of 35 weeks. The controls were 39 term pregnant women underwent selective cesarean section during the research duration and had no undergoing diseases and complications. The age covered 23 years to 38 years with a median of 28.0 years and their gestational ages at delivery covered 31 weeks to 42 weeks with a median of 39 weeks. Fasting blood samples were taken from all the patients and controls and sera were collected andstored at -30°C until assayed. Placenta samples were taken immediately after it was delivered and was washed with cold saline, absorbed with paper towels, snap-frozen in liquid nitrogen and stored at -30 °C until assayed. To make placental homogenate, placental samples were thawed on ice and 2.5 volumes of extraction buffer were added. Placentas were homogenized, centrifuged and the supernatant was collected for the assays of protein and CRH. CRH in serum and placental homogenate were determined by means of ELISA and protein by the method of Bradford. Placental CRH levels were expressed in pmol per g protein.From our data, we showed for the first time an extremely low CRH levels in maternal serum in preeclampsia group compared with that of controls (P0.05). It seemed that, whenever in mild or severe preeclampsia, the concentrations of CRH in both serum and placenta were at the same level (P>0.05).When preeclampsia patients were divided into three groups according to their gestational weeks of preeclampsia onset: before 32 complete weeks, after 32 weeks but before 37 complete weeks, after 37 weeks, placental levels of CRH were not significantly different (P>0.05). But in serum, levels of CRH with the disease onset before 32 complete weeks were significantly lower than that after 37 weeks (PO.05).Above all, the levels of serum CRH decreased significantly in preeclampsia and no changes occurred in the placental CRH, and these changes are not correlated with severity of the disease. We can thus conclude that the low level of maternal circulating CRH is an important pathological change in preeclampsia, and may play a role in the progress of the disease. On the other hand, the discrepancy of changes in circulatingand placental CRH levels in preeclampsia indicates the complicacy of the etiology and pathogenesis of preeclampsia.