Endothelial vasoactive mediators in preeclampsia,

https://doi.org/10.1016/0002-9378(93)90154-BGet rights and content

Objective: In recent years an increasing amount of evidence supports the concept that preeclampsia is an endothelial disease. The purpose of our study was to evaluate the extent to which endothelial cell dysfunction is involved in the pathophysiology of preeclampsia.

Study Design: We studied the urinary excretion of thromboxane B2 and 6-keto-prostaglandin F and the venous plasma endothelin levels in 23 preeclamptic patients and in control subjects. In six of these patients and in six controls arterial plasma endothelin levels were also measured. In addition, plasma levels of calcitonin gene-related peptide and plasma fibronectin levels were measured. Results were analyzed by Wilcoxon's rank-sum test or signed-rank test.

Results: In preeclampsia the urinary thromboxane B2/6-keto-prostaglandin F ratio (p < 0.001), venous plasma endothelin levels (p < 0.001), and plasma fibronectin levels (p < 0.001) were significantly elevated compared with normotensive pregnancy. Arterial plasma endothelin levels were significantly higher than venous plasma endothelin levels in normotensive and hypertensive patients (p < 0.05). Calcitonin gene-related peptide levels showed a wide range in normotensive pregnancy and in preeclampsia, but the difference was not significant.

Conclusions: These results confirm the extensive involvement of the endothelium in the pathophysiology of preeclampsia. Preeclamptic vasoconstriction seems to be mediated by an increase in the vasoconstrictor autocoids thromboxane A2 and endothelin. Production of prostacyclin by the vessel wall and endovascular trophoblast might be just a pivotal escape mechanism of the uteroplacental circulation. Calcitonin gene-related peptide appears not to be involved in the pathophysiology of preeclampsia.

References (25)

Cited by (106)

  • Placental Endocrine Function and Hormone Action

    2015, Knobil and Neill's Physiology of Reproduction: Two-Volume Set
  • Circulating calcitonin gene-related peptide and its placental origins in normotensive and preeclamptic pregnancies

    2006, American Journal of Obstetrics and Gynecology
    Citation Excerpt :

    Furthermore, our data indicated that both maternal and fetal plasma CGRP positively correlated with fetal birth weight, suggesting that in pregnancy, CGRP may be involved in the regulation of uteroplacental blood flow. However, few other reports indicated that maternal and fetal plasma CGRP levels in preeclampsia did not significantly differ from maternal and fetal CGRP levels of normal pregnancies,16 possibly due to a wide range of values observed in both groups. In another report,17 the data failed to demonstrate a difference in plasma CGRP levels between nonpregnant and pregnant women despite the well-known increase of CGRP in maternal plasma in pregnancy.18

  • Shared and disparate components of the pathophysiologies of fetal growth restriction and preeclampsia

    2006, American Journal of Obstetrics and Gynecology
    Citation Excerpt :

    During pregnancy, accelerated endothelial dysfunction is a central feature of both preeclampsia and IUGR. Endothelial activators such as vascular cellular adhesion molecule-1 (VCAM), intercellular adhesion molecule-1 (ICAM), endothelin-1, cellular fibronectin, and E-selectin are elevated in the maternal serum and plasma of women with both conditions,29-36 although activator levels in preeclampsia exceed those observed in IUGR. Markers of endothelial dysfunction are evident months before the clinical recognition of preeclampsia.30

View all citing articles on Scopus

Supported by grants from Organon International.

Presented at the Twelfth Annual Meeting of the Society of Perinatal Obstetricians, Orlando, Florida, February 3–8, 1992.

a

From the Department of Obstetrics and Gynecology Chemistry, Free University Hospital.

b

From the Department of Clinical Chemistry, Free University Hospital.

View full text