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

1991; Elsevier BV; Volume: 165; Issue: 6 Linguagem: Inglês

10.1016/0002-9378(91)90021-i

1097-6868

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

Cardiovascular Issues in Pregnancy

The vasoconstrictor peptide endothelin-1 (8 x 10-10 to 1 x 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 SQ29548 (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. (AM J OBSTET GYNECOL 1991;165:1717-22.)