LEVELS OF PROOPIOMELANOCORTIN AND PROLACTIN MESSENGER-RNA IN THE FETAL SHEEP PITUITARY FOLLOWING HYPOXEMIA AND GLUCOCORTICOID TREATMENT IN LATE-GESTATION
Sg. Matthews et Jrg. Challis, LEVELS OF PROOPIOMELANOCORTIN AND PROLACTIN MESSENGER-RNA IN THE FETAL SHEEP PITUITARY FOLLOWING HYPOXEMIA AND GLUCOCORTICOID TREATMENT IN LATE-GESTATION, Journal of Endocrinology, 147(1), 1995, pp. 139-146
It is well established that corticotrophin-releasing hormone and vasop
ressin can induce both synthesis and release of ACTH from the ovine pi
tuitary gland, and that glucocorticoids can inhibit these responses. C
hanges in the abundance, localization and distribution of proopiomelan
ocortin (POMC) mRNA and prolactin (PRL) mRNA in the ovine fetal pituit
ary were examined by in situ hybridization following hypoxaemia applie
d in the presence or absence of concomitant cortisol in late gestation
(day 135). Fetuses were distributed amongst four groups; saline-infus
ed/normoxaemic, cortisol-infused/normoxaemic (0.3 mg/h), saline-infuse
d/hypoxaemic and cortisol-infused/hypoxaemic. Hypoxaemia (6 h) was ind
uced by reducing the maternal PaO2, resulting in a 6-8 mmHg decrease i
n fetal arterial PO2. Fetal infusions were commenced 5 h prior to and
maintained throughout the treatment period. Hypoxaemia, which elevated
fetal plasma ACTH and cortisol, caused a significant (P<0.05) increas
e in POMC mRNA in the pars distalis (PD), but was without effect on PO
MC mRNA in the pars intermedia (PI). Cortisol infusion attenuated the
hypoxaemia-induced increase in POMC mRNA in the PD, but was without ef
fect on non-stimulated steady-state POMC mRNA levels in either the PD
or PI. PRL mRNA was only present in the PD and significantly (P<0.05)
increased after cortisol infusion and hypoxaemia. In conclusion (i) PO
MC and PRL mRNA in the PD are increased following moderate hypoxaemia,
(ii) cortisol attenuates changes in POMC mRNA but not PRL mRNA in the
PD following hypoxaemia and (iii) cortisol increases PRL mRNA levels
in the PD. Synthesis of POMC and PRL in the fetal PD is highly sensiti
ve to homeostatic perturbations and glucocorticoids in late gestation.