Abstract.
The LH releasing activities of LRH and the LRH-analogue buserelin® (HOE 766; (D-Ser (But)6-LRH(1–9)nona peptide-ethylamide) were compared in intact and short- and long-term castrated male rats, pre-treated (either 1 or 3 days) with oestradiol benzoate (EB) or oil.
LRH and buserelin were infused iv at the constant rate of 104 ng/h for 21 h. Blood samples were taken from an intracarotid cannula. LH responses were judged on the basis of the mean maximal height of the LH concentration (MH; ng LH/ml plasma) and a parameter of total LH release, i.e. the area under the curve of LH concentrations plotted against time ('area under the curve', AUC; expressed in 'area units'). The release efficiency of LRH and buserelin, E (see for a definition: Materials and Methods), which informs on the total quantity of LH released in relation to pituitary LH content, was calculated by dividing the AUC × 100 by the pituitary LH content at the beginning of stimulation.
Maximal plasma LH concentrations were observed between t= 1.5 and t=3 h after LRH and between t= 1.5 and t=9 after buserelin treatment. Both with LRH and buserelin the rise of LH secretion was greater the longer the animals were castrated and/or pre-treated with EB. The buserelin-induced LH response (with the exception of the responses induced in the EB-pre-treated, 4-weeks castrated rat) were about 2–2.5 times higher (MH) and larger (AUC) than the corresponding LRH-induced responses. The buserelin/LRH potency ratio, therefore, is about 2–2.5.
EB-pre-treatment did not change the pituitary LH content. It therefore enhanced the efficiency of release of LH of both LRH and buserelin. Castration, on the other hand, caused an increase of the pituitary LH content: after 4 weeks it was raised by a factor 4. Since, however, the LH responses induced by LRH and buserelin were proportionally higher and larger, castration did not significantly change the efficiency of LH release.
The results indicate that the efficiency of LH release can be changed by changes in the endocrine environment in the experimental animals, whilst for the magnitude of LH responses the pituitary LH content is also important. It is therefore suggested that the responsiveness of the pituitary gland to LRH (and agonistic analogues) is determined by (1) the state of the LH secretion mechanism and (2) the pituitary LH content.
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