Corticotropin-releasing hormone-induced vasodilatation in the human fetal placental circulation

J Clin Endocrinol Metab. 1994 Aug;79(2):666-9. doi: 10.1210/jcem.79.2.8045990.

Abstract

The vasoactive effects of corticotropin-releasing hormone (CRH) in the human fetal-placental circulation in vitro have been investigated. Single lobules of term placentae were bilaterally perfused with constant flows of Krebs' solution (maternal and fetal, 5 ml/min, 95% O2, 5% CO2, 37 degrees C, pH 7.3) and changes in fetal-placental arterial perfusion pressure measured. Effects of human (hCRH) and ovine (oCRH) CRH were examined during submaximal vasoconstriction (100-120 mmHg) of the fetal-placental vasculature induced by prostaglandin F2 alpha (PGF2 alpha), (0.7-2 mumol/L). During infusion of hCRH or oCRH (24-7000 pmol/L) a concentration-dependent vasodilatation was observed. Human CRH and oCRH were equipotent as vasodilator agents (regression analysis; P > 0.05; n = 5). The vasodilator response curves to human and ovine CRH were compared to prostacyclin (PGI2) (1.2-1180 nmol/L). Human and oCRH were 53 times more potent than PGI2 (regression analysis, P < 0.05; n = 5). These results indicate that CRH has powerful vasodilator properties in the human fetal-placental circulation and may play a role in control of placental vascular resistance to blood flow.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Corticotropin-Releasing Hormone / pharmacology*
  • Dinoprost / pharmacology
  • Epoprostenol / pharmacology
  • Female
  • Fetus / blood supply*
  • Humans
  • Placenta / blood supply*
  • Pregnancy
  • Vasodilation / drug effects*

Substances

  • Corticotropin-Releasing Hormone
  • Dinoprost
  • Epoprostenol