Corticotropin-Releasing Hormone and Oxytocin Stimulate the Release of Placental Proopiomelanocortin Peptides

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Abstract
Human placenta contains the POMC-derived peptides ACTH, aMSH, and β-endorphin, and CRH. High concentrations of immunoreactive (IR) CRH have been recently demonstrated in maternal plasma during pregnancy. To determine if the human placenta secretes CRH and POMC-derived peptides, we developed an in vitro human placental fragment perifusion system. The perifused tissue released IR-CRH and POMC-derived peptides at a constant rate for at least 5 h. The mean IR-CRH concentration in the effluent (under basal conditions) was 158 ± 26 (±sd) pg (34.5 ± 5.8 fmol)/5-min fraction·g tissue. IR-αMSH, IR-β-endorphin, and IR-ACTH were also released into the perifusion medium; the mean concentration of αMSH released was 24.6 ± 8 pg (14.8 ± 4.8 fmol)/fraction·g, that of ACTH was 2.9 ± 1.9 pg (0.65 ± 0.43 fmol)/fraction·g, and that of β-endorphin was 12.9 ± 6 pg (3.8 ± 1.7 fmol)/fraction·g. We examined the effects of human CRH, oxytocin, vasopressin, and dexamethasone on placental POMC peptide secretion. Five-minute pulses of 10−8 or 10−6 mol/L human CRH or oxytocin produced an immediate and dose-dependent increase in all POMC peptides in the effluent. A 5-min pulse of 10−8 or 10−6 mol/L vasopressin had no effect. A continuous 4-h exposure to 10−6 mol/L dexamethasone had no effect on either basal IR-CRH or POMC-derived peptide or their KCl-induced release. In conclusion, we found that 1) human placenta releases IR-CRH and POMC-derived peptides in vitro; this phenomenon seems to be independent of glucocorticoid control; 2) placental CRH may have a paracrine effect on placental POMC peptide release in addition to its possible action on maternal pituitary hormone release; and 3) oxytocin, but not vasopressin, stimulates placental POMC peptide release.

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