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Proton Pump Inhibitors Decrease Soluble fms-Like Tyrosine Kinase-1 and Soluble Endoglin Secretion, Decrease

Kenji Onda1, Stephen Tong2, Sally Beard1

  • 1From the Translational Obstetrics Group, Department of Obstetrics and Gynaecology, Mercy Hospital for Women, University of Melbourne, Heidelberg, Victoria, Australia (K.O., S.T., S.B., N.B., F.B., R.H., L.T., K.P., T.K.-L., N.J.H.); Department of Clinical Pharmacology, Tokyo University of Pharmacy and Life Sciences, Hachioji, Japan (K.O., T.H.); Research Institute for Microbial Diseases, Osaka University, Japan (M.M., M.I.); School of Biosciences, University of Melbourne, Parkville, Victoria, Australia (S.N.S., L.P.); Maternal and Fetal Health Research Centre, Institute of Human Development, University of Manchester, United Kingdom (M.D., L.R.); St Mary's Hospital, Central Manchester University Hospitals NHS Trust, Manchester Academic Health Science Centre, United Kingdom (M.D., L.R.).

Hypertension (Dallas, Tex. : 1979)
|January 25, 2017
PubMed
Summary

Proton pump inhibitors (PPIs) show promise for treating preeclampsia by reducing placental antiangiogenic factors, improving endothelial function, and lowering blood pressure. These findings suggest PPIs could be a safe and effective therapeutic option for preeclampsia.

Keywords:
hypertensionpreeclampsiapregnancyproton pump inhibitorstherapeutics

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Area of Science:

  • Obstetrics and Gynecology
  • Pharmacology
  • Cardiovascular Research

Background:

  • Preeclampsia is a severe pregnancy complication characterized by hypertension and endothelial dysfunction.
  • Excess placental secretion of antiangiogenic factors, such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin, contributes to preeclampsia's pathophysiology.
  • Oxidative stress and vascular inflammation worsen endothelial injury in preeclampsia.

Purpose of the Study:

  • To investigate the therapeutic potential of proton pump inhibitors (PPIs) for preeclampsia.
  • To examine the effects of PPIs on sFlt-1 and soluble endoglin secretion, blood pressure, and endothelial function.

Main Methods:

  • Functional studies were conducted on primary human tissues and animal models.
  • Assessed PPI effects on sFlt-1 and soluble endoglin secretion from placental and endothelial cells.
  • Evaluated PPIs' impact on endothelial dysfunction, vasodilation, blood pressure, and inflammatory markers.

Main Results:

  • PPIs reduced sFlt-1 and soluble endoglin secretion and mitigated tumor necrosis factor-α-induced endothelial dysfunction.
  • Esomeprazole, a PPI, demonstrated vasodilation in maternal blood vessels and decreased blood pressure in a preeclampsia mouse model.
  • PPIs exhibited antioxidant and anti-inflammatory properties, upregulating antioxidant defenses and decreasing cytokine secretion.

Conclusions:

  • PPIs effectively decrease key preeclampsia-related factors and improve endothelial function.
  • PPIs possess vasodilatory, antihypertensive, antioxidant, and anti-inflammatory properties.
  • PPIs represent a potential therapeutic strategy for preeclampsia and other endothelial dysfunction-related diseases.