The effects of sexual maturation and altered steroid synthesis on the production and route of secretion of inhibin-alpha from the rat testis.
This study has determined the route of secretion of inhibin-alpha into blood by the rat testis during sexual maturation, and in adult animals in which Leydig cell steroidogenesis was stimulated with human CG (hCG) or suppressed with aminoglutethimide. In each rat, inhibin-alpha levels were measured in samples of testicular (TV), spermatic (SV), and peripheral (PV) venous blood plasma, and in testicular interstitial fluid (IF). The IF and TV plasma reflect inhibin-alpha secretion via the base of the Sertoli cell while that secreted via the apex of the Sertoli cell (which is resorbed from the rete testis) was determined from the difference between SV and TV levels of inhibin-alpha. During sexual maturation, inhibin-alpha levels in IF and all plasma samples declined from maximal values at 28 days of age to minimal values at 100 days of age, in contrast to testosterone levels which showed the reverse pattern. There was a major change with age in the route of secretion of inhibin-alpha from the testis into blood. In immature (28-35 days) rats, most inhibin-alpha (58-65%) leaving the testis in blood was derived from that secreted via the base of the Sertoli cell with a relatively small contribution (35-42%) from apically-secreted inhibin-alpha. However, the latter made a progressively increasing contribution between 45 and 100 days of age (adults) and in adult rats the vast majority of inhibin-alpha (95%) leaving the testis in blood was derived from apically-secreted inhibin-alpha. This change was due primarily to a progressive reduction with age in the secretion of inhibin-alpha via the base of the Sertoli cell, a change which was confirmed by inhibin bioassay. Stimulation of steroidogenesis in the adult testis with hCG significantly increased inhibin-alpha and testosterone levels in IF and all plasma samples. The concomitant administration of hCG and aminoglutethimide (to block steroidogenesis) prevented the hCG-induced increase in testosterone levels, but still led to significant increases in inhibin-alpha secretion which were comparable to those seen with the use of hCG alone. The administration of aminoglutethimide (AMG) on its own did not alter the inhibin-alpha secretion profile from that seen in controls, but it did significantly reduce the levels of testosterone in all fluids. In rats treated with hCG +/- AMG there was a small change in the route of secretion of inhibin-alpha into blood, with an increased contribution (24-37%) from inhibin-alpha secreted via the base of the Sertoli cell, when compared with controls (7-16%).(ABSTRACT TRUNCATED AT 400 WORDS)
Maddocks
S
S
MRC Reproductive Biology Unit, Centre for Reproductive Biology, Edinburgh, Scotland, United Kingdom.
Sharpe
R M
RM
D000616:Aminoglutethimide / Q000494:pharmacology; D000818:Animals; D006063:Chorionic Gonadotropin / Q000494:pharmacology; D007265:Inhibins / Q000378:metabolism*; D007985:Leydig Cells / Q000378:metabolism; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012741:Sexual Maturation / Q000502:physiology*; D013256:Steroids / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D013737:Testis / Q000378:metabolism*; D013739:Testosterone / Q000378:metabolism
D006063:Chorionic Gonadotropin; D013256:Steroids; D000616:Aminoglutethimide; D013739:Testosterone; D007265:Inhibins