Abstract

As a part of a series of studies on the regulation of testicular steroidogenesis in the fetal rat, we found that VIP stimulated fetal testicular cAMP production at a dose of 10 −9 mol/l, while a dose as low as 10 −12 mol/l stimulated testosterone production. RT-PCR analysis could not reveal either VIP mRNA in fetal tissues or VIP1 receptor mRNA in the fetal or newborn testes, while VIP2 receptor mRNA was detected in fetal testes as early as E15.5. The testicular VIP content was unmeasurable by our radioimmunoassay method (<1 fmol/testis), while the circulating levels of VIP were 82.9±1.1 pmol/l at E17.5 and decreased with advanced fetal ages. In conclusion, our results suggest that VIP, from and extratesticular source, may regulate fetal testicular steroidogenesis through type 2 receptors as early as E15.5.

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