Endothelin-1-induced vasoconstriction is not mediated by thromboxane release and action in the human fetal-placental circulation

Leslie Myatt, Gretchen Langdon, Anthony S. Brewer, Diane E. Brockman

Research output: Contribution to journalArticle

28 Scopus citations

Abstract

The vasoconstrictor peptide endothelin-1 (8 × 10-10 to 1 × 10-8 mol/L) significantly increased fetal-placental perfusion pressure in vitro in a cumulative manner from 30 ± 2 to 123 ± 25 mm Hg (mean ± SEM, n = 5, p < 0.0005, analysis of variance). Accompanying this vasoconstriction was a corresponding reduction in fetal-placental perfusate flow rate. Measurement of thromboxane B2 and 6-keto-prostaglandin F in the fetal-placental perfusate revealed a significant reduction in their release (p < 0.0096 and p < 0.0004, analysis of variance, respectively) when corrected for flow rate. Neither the thromboxane synthesis inhibitor dazoxiben (10-6 mol/L) nor the thromboxane receptor antagonist SO29548 (10-6 mol/L) was able to block the vasoconstrictor actions of endothelin-1. Therefore endothelin-1-induced vasoconstriction in the human fetal-placental circulation does not appear to be mediated by thromboxane release or action. The stimulus to eicosanoid release in the fetal-placental circulation may be hydrodynamic, i.e., flow or shear stress.

Original languageEnglish (US)
Pages (from-to)1717-1722
Number of pages6
JournalAmerican journal of obstetrics and gynecology
Volume165
Issue number6 PART 1
DOIs
StatePublished - Dec 1991

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Keywords

  • Endothelin
  • hromboxane
  • placenta
  • vasoconstriction

ASJC Scopus subject areas

  • Obstetrics and Gynecology

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