CORTICOTROPIN-RELEASING HORMONE-INDUCED VASODILATATION IN THE HUMAN FETAL-PLACENTAL CIRCULATION

The vasoactive effects of corticotropin-releasing hormone (CRH) in the human fetal-placental circulation in vitro have been investigated. Si ngle lobules of term placentae were bilaterally perfused with constant flows of Krebs' solution (maternal and fetal, 5 ml/min, 95% O-2, 5% C O2, 37 degrees C, pH 7.3) and changes in fetal-placental arterial perf usion pressure measured. Effects of human (hCRH) and ovine (oCRH)) CRH were examined during submaximal vasoconstriction (100-120 mmHg) of th e fetal-placental vasculature induced by prostaglandin F2 alpha (PGF(2 ) alpha), (0.7-2 mu mol/L). During infusion of hCRH or oCRH (24-7000 p mol/L) a concentration-dependent vasodilatation was observed. Human CR H 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 (PGI(2)) (1.2-1180 nmol/L), Human and oC RH were 53 times more potent than PGI(2) (regression analysis, P<0.05; n=5). These results indicate that CRH has powerful vasodilator proper ties in the human fetal-placental circulation and may play a role in c ontrol of placental vascular resistance to blood flow.