Prostaglandin E2 releases ovine fetal ACTH from a site not perfused by the carotid vasculature.
Placental prostaglandin E2 (PGE2) is thought to influence the ovine fetal adrenocortical system to control the timing of parturition. We investigated whether physiological infusions of PGE2 increase fetal immunoreactive adrenocorticotropin (iACTH) at the fetal brain or pituitary or at a site not perfused by the carotid vasculature. PGE2 was infused into the carotid artery (ica) at 0 (n = 5), 10 (n = 5), or 100 ng/min (n = 4) or into the vena cava (ivc) at 10 (n = 5) or 100 ng/min (n = 5) for 30 min in fetuses between 119 and 130 days gestation. Blood gases, vasopressin, cortisol, and arterial and central venous pressure were unchanged. Heart rate increased only in the 100 ng/min ica group. iACTH increased only in the 100 ng/min ivc group from 59 +/- 26 to 180 +/- 73 pg/ml. We conclude that PGE2 infused to create physiological plasma concentrations similar to those at the end of gestation stimulates iACTH from a site other than the fetal brain or pituitary.
Cudd
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Department of Physiology, University of Florida, Gainesville 32610.
Wood
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D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood; D002339:Carotid Arteries / Q000502:physiology*; D015232:Dinoprostone / Q000494:pharmacology*; D004573:Electrolytes / Q000097:blood; D005333:Fetus / Q000378:metabolism*; D006339:Heart Rate / Q000187:drug effects; D011863:Radioimmunoassay; D012039:Regional Blood Flow; D012756:Sheep
D004573:Electrolytes; D001127:Arginine Vasopressin; D000324:Adrenocorticotropic Hormone; D015232:Dinoprostone