Endocrinology · 1969 · 57 citations · 0 references
Life SciencesEndocrinologyPhysiologyReproductive EndocrinologyReproductive PhysiologySteroid BiochemistryMammalian EndocrinologyPituitary Gland FunctionPituitary Hormone RegulationPituitary HormonesRodent EndocrinologyPituitary Hormone AssaysPituitary Hormone BiochemistryPituitary Physiology
The effects of short-term steroid treatment on the blood and pituitary LH and FSH levels of previously castrated adult male and female rats were examined, using ovarian ascorbic acid depletion (OAAD) and HCG-augmentation bioassays for LH and FSH activities. Pituitary and plasma FSH activities, 3 days after an injection of 1) testosterone propionate (TP) or 2) estradiol benzoate plus progesterone (E + P), were compared in 5 experiments. Concomitant changes in plasma and pituitary LH levels were studied in 3 of these experiments and 2 others. In 2 further studies in spayed rats, both stored and circulating LH and FSH were examined after 7 days of TP treatment. In addition, pituitary FSH and plasma LH were studied 24 hr after single injections of TP. Both steroid treatments (TP and E + P) decreased plasma LH levels without altering pituitary LH concentrations detectably. The TP effect on plasma LH was evident after only 24 hr. Thus, both treatments apparently reduced the rate of LH release. Because of the relatively long pituitary turnover time for LH in the castrated rat, however, no conclusions can yet be drawn about whether these short-term treatments also influenced LH synthesis. The 2 steroid treatments clearly differed in their effects on FSH secretion. Pituitary FSH stores were increased after 1, 3 or 7 days of TP treatment while plasma FSH concentrations were not altered significantly. By contrast, the E + P treatment consistently lowered plasma FSH titers without appreciably altering pituitary FSH stores. In the TP-treated castrate, therefore, plasma FSH levels need not decrease detectably for pituitary FSH concentration to increase. The differences between 1) the ability of TP to elevate pituitary FSH content without decreasing plasma FSH activity, and 2) the ability of E + P to lower plasma FSH levels without altering pituitary FSH stores, cannot be accounted for solely on the basis of altered FSH release. One or both of these treatments must affect the rate of FSH synthesis. Calculations based on our recent estimate of the pituitary FSH secretory rate and turnover time in the untreated castrate show that the E + P treatment impairs both the synthesis and release of FSH. Similar calculations show that long-term TP treatment also reduces the rate of FSH synthesis, but that neither the extent nor direction of any short-term TP effects on FSH synthesis can yet be evaluated. (Endocrinology84: 1132, 1969)