Adrenocortical responses to adrenocorticotrophin in the hypophysectomized ovine fetus.
Fetal adrenocortical responsiveness to ACTH declines during 90-120 days gestation and fetal pituitary peptides have been implicated in this refractoriness. In these studies the ACTH-induced cortisol responses were measured in 11 ovine fetuses of 114 days gestation. Five animals were hypophysectomized as evidenced by prolonged gestation, pituitary histology, TRH-testing, delayed maturation and decreasing fetal plasma prolactin concentrations (less than 1 ng.ml-1) (P less than 0.005). Resting cortisol concentrations decreased from 22.4 to 8.1 ng.ml-1 in the hypophysectomy group and were not different from the control group (19.6-14.9 ng.ml-1) over the 5 days of study. Responses measured as increments in plasma cortisol concentrations increased equally and successively in both groups. Since pituitary ablation fails to enhance fetal adrenal responsiveness to ACTH we conclude that refractoriness is unlikely to be caused by an inhibitor of pituitary origin.
D000302:Adrenal Cortex / Q000187:drug effects* / Q000196:embryology / Q000378:metabolism; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D005260:Female; D005333:Fetus / Q000187:drug effects* / Q000502:physiology; D005865:Gestational Age; D006854:Hydrocortisone / Q000097:blood; D010902:Pituitary Gland / Q000502:physiology*; D011247:Pregnancy; D011388:Prolactin / Q000097:blood; D012756:Sheep
D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D006854:Hydrocortisone