Short-term effects of glucocorticoids in the human fetal-placental circulation in vitro

Abstract

A number of studies demonstrate that both long-term and short-term exposure to glucocorticoids alters vascular function. We have examined whether the short-term administration of glucocorticoids into the human fetal-placental circulation affects placental arterial pressure and alters vascular responses to vasoconstrictive and vasodilator agents. Single lobules of term human placentae were bilaterally perfused in vitro with Krebs’ solution (maternal and fetal, 5 ml/min Krebs, 95% O2, 5% CO2, 37 C, pH 7.3), and changes in fetal-placental arterial perfusion pressure were measured. Dexamethasone (100 nM) infusion for 1 h into the fetal-placental circulation caused a significant decrease in basal arterial pressure (n = 19, t test, P < 0.05). Continuous dexamethasone infusion (100 nM) did not alter vasoconstrictive responses to PGF2{alpha} (0.5–120 pM, n = 12, ANOVA, P > 0.05) or potassium chloride (5–600 mM, n = 12, ANOVA, P > 0.05) or vasodilator responses to CRH (53–7400 pM, n = 13, ANOVA, P > 0.05). However when fetal-placental vessels were submaximally preconstricted and then infused with dexamethasone alone (40 nM–10 µM), there was a dose-dependent decrease in arterial pressure (n = 8). Dexamethasone-induced dilation was not inhibited by blocking nitric oxide synthase or cyclo-oxygenase activity. These data suggest that dexamethasone can cause dilation in the fetal-placental circulation, possibly via an endothelium-independent pathway.