title: Circulating concentrations of dimeric inhibin A and B in the male rhesus monkey (Macaca mulatta).
abstract: 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.
authors.affiliation: Department of Cell Biology and Physiology, University of Pittsburgh School of Medicine, Pennsylvania 15261, USA.
authors.forename: T M
authors.initials: TM
authors.lastname: Plant
authors.forename: V
authors.initials: V
authors.lastname: Padmanabhan
authors.forename: S
authors.initials: S
authors.lastname: Ramaswamy
authors.forename: D S
authors.initials: DS
authors.lastname: McConnell
authors.forename: S J
authors.initials: SJ
authors.lastname: Winters
authors.forename: N
authors.initials: N
authors.lastname: Groome
authors.forename: A R
authors.initials: AR
authors.lastname: Midgley
authors.forename: A S
authors.initials: AS
authors.lastname: McNeilly
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000097:blood; D019281:Dimerization; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007118:Immunoassay; D007265:Inhibins / Q000097:blood*; D008163:Luminescent Measurements; D008253:Macaca mulatta; D008297:Male; D009919:Orchiectomy; D012016:Reference Values; D013737:Testis / Q000098:blood supply / Q000502:physiology
chemical_list: D007265:Inhibins