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Experimental Studies |
Departments of Cell Biology and Physiology (T.M.P., S.R.) and Medicine (S.J.W.), University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261; Reproductive Sciences Program (D.S.McC., A.R.M.), University of Michigan, Ann Arbor, Michigan 48109; Oxford Brooks University (N.G.), Oxford, OX3 0BP, United Kingdom; and the Medical Research Council Reproductive Biology Unit (A.S.McN.), University of Edinburgh, 37 Chalmer Street, Edinburgh EH3 9EW, United Kingdom
Address all correspondence and requests for reprints to: Tony M. Plant, Departments of Cell Biology and Physiology, University of Pittsburg School of Medicine, S330 Biomedical Science Tower, 3500 Terrace Street, Pittsburg, Pennsylvania, 15261.
The purpose of this study was to determine the relative concentrations of inhibin A and B in peripheral serum of the adult male rhesus monkey and to examine the testicular contribution to these circulating forms of inhibin. In addition, inhibin B concentrations were also determined in peripheral sera of neonatal and juvenile males and in spermatic vein blood of adults. Immunoradiometric assays specific for the measurement of inhibin A and B were used. These assays also provided an opportunity to reexamine the physiological significance of a replacement infusion of recombinant human (rh)-inhibin A previously employed to study the role of this hormone in regulating FSH secretion in the monkey. In intact adults, the mean (± SE) serum concentration of inhibin B was 1008 ± 184 pg/mL. In contrast, circulating inhibin A concentrations were very low (<46 pg/mL). Inhibin B was consistently detected in neonatal monkey serum (275 ± 57 pg/mL), and concentrations of this inhibin dimer increased throughout postnatal development, reaching maximum values in adulthood. Circulating inhibin A concentrations in neonatal and juvenile monkeys were undetectable (<7 pg/mL). Both forms of inhibin were generally undetectable in castrate sera. The ratio of inhibin B concentrations in testicular venous blood to those in the peripheral circulation was 1.4:1. These findings indicate that, in the male monkey, inhibin B is the principal form of circulating dimeric inhibin, and that this hormone is derived exclusively from the testis. The elevated levels of circulating inhibin B in the juvenile male monkey suggest that, during this phase of development, testicular inhibin B secretion is relatively gonadotropin independent. Additionally, we found that the concentration of circulating inhibin A in castrate animals that had earlier received an iv infusion of rh-inhibin A (832 ng/h/kg BW) was 9881 ± 2135 pg/mL, indicating that this mode of inhibin replacement may not have been entirely physiological.
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