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The nitric oxide pathway in pre-eclampsia: pathophysiological implications

I A Buhimschi1, G R Saade, K Chwalisz

  • 1The University of Texas Medical Branch, Department of Obstetrics and Gynaecology, Galveston 77555-1062, USA.

Human Reproduction Update
|June 11, 1998
PubMed
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Pre-eclampsia may stem from a deficiency in nitric oxide (NO), a crucial molecule in pregnancy. Further research is needed to clarify NO's role in human pregnancy adaptation and its interaction with other free radicals.

Area of Science:

  • Obstetrics and Gynecology
  • Cardiovascular Physiology
  • Free Radical Biology

Background:

  • Pre-eclampsia affects 6-8% of pregnancies, causing significant maternal and infant mortality.
  • Free radicals are increasingly implicated in the pathophysiology of pre-eclampsia.
  • Nitric oxide (NO) plays a vital role in reproductive tissues and blood vessels during pregnancy.

Purpose of the Study:

  • To review the biochemistry of nitric oxide (NO).
  • To explore the interactions between NO and other free radicals in pre-eclampsia.
  • To investigate the potential of NO deficiency as a cause of pre-eclampsia.

Main Methods:

  • Review of existing literature on nitric oxide (NO) biochemistry and its role in pregnancy.
  • Examination of studies using rat models of pre-eclampsia, including NO synthase inhibition with L-NAME.

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  • Analysis of the effects of steroid hormones on blood pressure in animal models.

    • Main Results:

    • Pregnancy in rats is associated with increased NO production and responsiveness.
    • Animal models suggest pre-eclampsia may be linked to a deficiency in NO.
    • Human studies show conflicting results regarding NO's involvement in maternal adaptation to pregnancy.

    Conclusions:

    • Pre-eclampsia might be characterized by a deficiency in nitric oxide (NO).
    • NO may be one of several systems maintaining the mother-fetus symbiosis.
    • The contribution of each system, including NO, could be genetically determined.