Vascular function in preeclampsia

Cardiovasc Res. 2000 Jul;47(1):38-48. doi: 10.1016/s0008-6363(00)00087-0.

Abstract

Preeclampsia is a multisystem disorder peculiar to human pregnancy. It occurs in 4-5% of all pregnancies and remains a leading cause of maternal and neonatal mortality and morbidity. The pathophysiology of this syndrome is not fully understood. Two stages of vascular dysfunction seem to be involved. In the early stage suboptimal development of the placenta and a hemodynamic maladaptation to pregnancy exist. At this stage maternal constitutional factors such as genetic and immunological factors and pre-existing vascular diseases may play a role. Due to this defective placentation a factor is released from the placenta, supposedly under the influence of ischemia. This factor then results in the late vascular dysfunction characterised mainly by a generalised endothelial dysfunction, leading to the clinical syndrome of preeclampsia. This review attempts to unravel the mechanisms that may contribute to preeclampsia-associated changes in vascular function and to indicate the research needed to improve our understanding of this disease.

Publication types

  • Review

MeSH terms

  • Adult
  • Arteries
  • Atrial Natriuretic Factor / metabolism
  • Endothelial Growth Factors / metabolism
  • Endothelium, Vascular / physiopathology*
  • Epoprostenol / metabolism
  • Female
  • Genotype
  • Humans
  • Lymphokines / metabolism
  • Muscle, Smooth, Vascular / physiopathology
  • Placenta / blood supply*
  • Pre-Eclampsia / etiology
  • Pre-Eclampsia / immunology
  • Pre-Eclampsia / physiopathology*
  • Pregnancy
  • Thromboxane A2 / metabolism
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Vasoconstriction

Substances

  • Endothelial Growth Factors
  • Lymphokines
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Thromboxane A2
  • Atrial Natriuretic Factor
  • Epoprostenol