Contribution of the fetal adrenal to circulating immunoactive inhibin in the chicken embryo.
High concentrations of immunoactive inhibin are observed in the plasma of male and female chicken embryos. The exact nature and the source of this material remain obscure. In a previous study we presented evidence that the fetal gonads are unlikely to be the main source of circulating inhibin (Biol Reprod 1993; 49:549-554). Here we demonstrate that the fetal adrenal may account for the major portion of circulating immunoactive inhibin in the chicken embryo. A comparison of the inhibin content of different fetal organs shows that, expressed per milligram of tissue, the adrenal ranks second. Only the testis has a higher inhibin content, while the inhibin content of the fetal ovary is considerably lower than that of the fetal adrenal. Suppression of endogenous ACTH secretion by administration of dexamethasone results in a marked decrease of plasma inhibin. Maximal suppression (down to 24% and 25% of the control values in male and female embryos, respectively) was observed with the lowest dose of dexamethasone tested (1 microgram/egg). Dexamethasone (100 microgram/egg) reduced testicular weight and testicular inhibin content to approximately 50% of the control value. It is unlikely, however, that this contributed significantly to the fall in circulating immunoactive inhibin. In fact, ovarian inhibin content was unaffected, but even so, a comparable drop in circulating inhibin was observed in female embryos. Dexamethasone caused only marginal changes in plasma FSH. Administration of a synthetic peptide with ACTH activity (Synacthen) in vivo did not produce measurable changes in circulating inhibin. Isolated and cultured fetal adrenal cells, however, produced immunoactive inhibin, and this production was increased fivefold after stimulation with synthetic ACTH.(ABSTRACT TRUNCATED AT 250 WORDS)
Rombauts
L
L
Laboratory for Experimental Medicine and Endocrinology, Onderwijs & Navorsing, Catholic University of Leuven, Gasthuisberg, Belgium.
Vanmontfort
D
D
Berghman
L R
LR
Decuypere
E
E
Verhoeven
G
G
D000311:Adrenal Glands / Q000196:embryology* / Q000378:metabolism / Q000502:physiology*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D002478:Cells, Cultured; D002642:Chick Embryo / Q000098:blood supply / Q000737:chemistry* / Q000378:metabolism; D003366:Cosyntropin / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D007265:Inhibins / Q000032:analysis* / Q000097:blood* / Q000378:metabolism; D008297:Male; D010053:Ovary / Q000737:chemistry / Q000196:embryology; D011863:Radioimmunoassay; D013737:Testis / Q000737:chemistry / Q000196:embryology
D003366:Cosyntropin; D007265:Inhibins; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D005640:Follicle Stimulating Hormone