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Journal of Andrology, Vol 6, Issue 2 77-82, Copyright © 1985 by The American Society of Andrology
JOURNAL ARTICLE |
M. O. Suescun, S. I. Gonzalez, V. A. Chiauzzi and R. S. Calandra
We have evaluated the effects of hypoprolactinemia during gonadal maturation in the male rat. Intact 30-day-old rats were injected daily for 10 days with three different doses of bromocriptine (0.75, 1.5 or 3.0 mg/kg of body weight/day). At the end of the treatment period, the animals were sacrificed, serum was collected for prolactin (PRL), LH, and androgen measurements. Intratesticular testosterone and 5 alpha-androstanediol (androstanediol) were measured following celite column chromatography and a specific radioimmunoassay. In addition, the production of androgens by decapsulated testes and dispersed Leydig cells was also studied in vitro. Serum levels of PRL (9.4 +/- 1.9 ng/ml) were suppressed to undetectable levels in the three bromocriptine-treated groups, whereas LH levels were not altered. All three doses of bromocriptine markedly depressed serum testosterone (plus DHT) and androstanediol. Intra-testicular testosterone and androstanediol were diminished (25% and 35%, respectively, P less than 0.05) during hypoprolactinemia. Decapsulated testes and dispersed Leydig cells from bromocriptine-treated animals showed a significant reduction in the basal secretion of testosterone (plus DHT) and androstanediol, and in androgen responses to submaximal hCG stimulation. Maximal steroidogenic responses from bromocriptine-treated rats were similar to controls. The present findings show that, during puberty, bromocriptine influences testicular steroidogenesis, and these effects may be partly due to changes in PRL levels. A direct effect of this dopaminergic agonist on the male gonad cannot be completely ruled out.
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