Targeting the vascular dysfunction

Potential treatments for preeclampsia

Sarah A. Marshall, Annie G. Cox, Laura J. Parry, Euan M. Wallace

Research output: Contribution to journalReview ArticleOtherpeer-review

1 Citation (Scopus)

Abstract

Preeclampsia is a pregnancy-specific disorder, primarily characterized by new-onset hypertension in combination with a variety of other maternal or fetal signs. The pathophysiological mechanisms underlying the disease are still not entirely clear. Systemic maternal vascular dysfunction underlies the clinical features of preeclampsia. It is a result of oxidative stress and the actions of excessive anti-angiogenic factors, such as soluble fms-like tyrosine kinase, soluble endoglin, and activin A, released by a dysfunctional placenta. The vascular dysfunction then leads to impaired regulation and secretion of relaxation factors and an increase in sensitivity/production of constrictors. This results in a more constricted vasculature rather than the relaxed vasodilated state associated with normal pregnancy. Currently, the only effective “treatment” for preeclampsia is delivery of the placenta and therefore the baby. Often, this means a preterm delivery to save the life of the mother, with all the attendant risks and burdens associated with fetal prematurity. To lessen this burden, there is a pressing need for more effective treatments that target the maternal vascular dysfunction that underlies the hypertension. This review details the vascular effects of key drugs undergoing clinical assessment as potential treatments for women with preeclampsia.

Original languageEnglish
Article numbere12522
Number of pages18
JournalMicrocirculation
Volume26
Issue number4
DOIs
Publication statusPublished - May 2019

Keywords

  • drug treatment
  • preeclampsia
  • vascular dysfunction

Cite this

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Targeting the vascular dysfunction : Potential treatments for preeclampsia. / Marshall, Sarah A.; Cox, Annie G.; Parry, Laura J.; Wallace, Euan M.

In: Microcirculation, Vol. 26, No. 4, e12522, 05.2019.

Research output: Contribution to journalReview ArticleOtherpeer-review

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