A continuous flow incubation (perifusion) system was used to' examine the effect of testosterone (T) and three of its 5α-reduced metabolites, dihydrotestosterone(DHT), 5α-androstane- 3α, 17β-diol (3α-Adiol) and its 3β-epimer (3β-Adiol) on LH and FSH release, induced by hypothalamic extract (HE). In the absence of steroids, successive identical pulses of HE, of 10 min duration each, administered at hourly intervals over a 8-hr period, caused highly reproducible release of LH and FSH. In experimental perifusions, the amounts of LH and FSH released in response to standard 10-min pulses of HE administered at hourly intervals during the continuous infusion of steroid for 4-6 hr were compared with the responses of the same pituitaries to the standard test pulses of HE givenbefore the start of the steroid infusion and after its cessation. All the androgens tested altered pituitary responsiveness. At the 0.1 and 1.0 μg/mldose level there were differences between the steroids in the way they influenced the responsiveness ofthe pituitary over time. Their effects at these two doses fell into three categories dependingon whether there was initially: 1) an augmentation of HE induced LH release (T and 3β-Adiol), 2) augmentation of both FSH and LH release (DHT), or 3) no augmentationinthe release of either gonadotrophin (3α-Adiol). All the androgens ultimately suppressedpituitary responsiveness to HE and all were associated with changes in the ratios of LH and FSH released. When the doseof T and 3β-Adiol was raised to 10 μg/ml or that of DHT lowered to 0.01 μg/ml the initial stimulatory phase was not seen. Epitestosterone, the biologically inactive epimer of T, did not alter the responsiveness of the pituitary of HE.
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