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 F1α 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 language | English (US) |
---|---|
Pages (from-to) | 1717-1722 |
Number of pages | 6 |
Journal | American journal of obstetrics and gynecology |
Volume | 165 |
Issue number | 6 PART 1 |
DOIs | |
State | Published - Dec 1991 |
Externally published | Yes |
Keywords
- Endothelin
- hromboxane
- placenta
- vasoconstriction
ASJC Scopus subject areas
- Obstetrics and Gynecology