Hormone ontogeny in the ovine fetus. XV. Studies of adenohypophysial hormones after fetal pituitary stalk section: evidence for an extrahypothalamic dopaminergic influence on fetal prolactin secretion.
The administration of a dopamine antagonist, haloperidol, to the ovine fetus in late gestation elevates plasma concentrations of PRL, suggesting tonic dopaminergic inhibition of fetal PRL secretion. The source of this dopaminergic inhibition was investigated in chronically catheterized ovine fetuses (104-135 days of gestation) after hypophysial stalk section (SS; n = 4) and in sham-operated controls (CON; n = 7). Basal PRL levels were similar in the two groups of fetuses. After the administration of TRF (250 micrograms, iv), PRL levels rose comparably in both the SS and CON fetuses. The only difference was a higher mean incremental response (P less than 0.02) in the SS fetuses. The dopamine agonist apomorphine (100 micrograms/kg, iv) induced a similar suppression of fetal PRL concentrations in CON (n = 4) and SS (n = 2) fetuses. After the administration of haloperidol (1 mg, iv) to the CON fetuses (n = 7), the concentration of fetal PRL rose (P less than 0.01). In the SS fetus (n = 4), haloperidol induced a rise in PRL concentrations (P less than 0.01); however, the response to haloperidol was less (P less than 0.01) in SS than in CON fetuses. These data suggest that there is persistent dopaminergic inhibition of PRL secretion in the fetus after complete stalk section, and that the source of this dopamine is extrahypothalamic. The greater incremental PRL response to TRH and the lesser response to haloperidol in the SS fetus than in CON are evidence for a hypothalamic component to the dopaminergic inhibition in the intact fetus. Basal FSH concentrations and the gonadotropin response to LRF were not affected by stalk section in fetuses studied 5-8 days after surgery. Both the PRL and the GH responses to 5-hydroxytryptophan were abolished by stalk section. After stalk section GH levels fell, however, significant concentrations of GH were measurable in fetal plasma in late gestation, which suggests that the fetal pituitary can secrete GH in the absence of hypothalamic stimulation at this stage in gestation.
D000818:Animals; D001058:Apomorphine / Q000494:pharmacology; D005260:Female; D005333:Fetus / Q000502:physiology; D006220:Haloperidol / Q000494:pharmacology; D007031:Hypothalamus / Q000196:embryology; D008297:Male; D010903:Pituitary Gland, Anterior / Q000187:drug effects / Q000196:embryology* / Q000378:metabolism; D010908:Pituitary Hormones, Anterior / Q000378:metabolism*; D011247:Pregnancy; D011388:Prolactin / Q000378:metabolism*; D012756:Sheep; D013973:Thyrotropin-Releasing Hormone / Q000494:pharmacology*
D010908:Pituitary Hormones, Anterior; D013973:Thyrotropin-Releasing Hormone; D011388:Prolactin; D006220:Haloperidol; D001058:Apomorphine