Biomedical subjects
Publications and source records attributed to E M Bogdanove.
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The original objective of this study was to use available distribution volume (V) and deca constant (k) estimates for rat LH and FSH to determine the amounts of these hormones synthesized and released during a dynamic secretory event, the postpartum preovulatory surge. The problem was approached by 1) determining the approximate rates and durations of pituitary LH and FSH depletion during the surge, and 2) comparing observed plasma LH and FSH patterns with patterns calculated on the assumptions a) that the rates and durations of LH and FSH release would have to equal or exceed the rates and durations of LH and FSH depletion, and b) that the V and k estimates reported by Bogdanove and Gay (Endocrinology 84: 1118, 1969) would be applicable in this situation. The observed surges proved to be 3- to 10-fold smaller than the calculated patterns, suggesting either that depletion exceded release or that inappropriate values of V and/or k had been used in the calculations. Subsequent reexaminations of LH clearance kinetics (Campbell et al., accompanying reports) provided larger estimates for both VLH and kLH. Recalculation of the data, using these new parameters, eliminated the apparent discrepancy between depletion and release. On the basis of these direct comparisons of stored and circulating LH, it seems that a "half-life" shorter than 30 min and a distribution volume greater than 3 ml/100 g must be used to model the effects of variations in LH release on circulating LH in the rat.
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Constant rate infusion/stop-entry experiments of varied duration were done with rat pituitary LH to test the possibility that the relatively slow disappearance of endogenous circulating LH after hypophysectomy/stop-entry in orchidectomized rats might be due to redistributive distortion consequent to a prolonged "packing" of the extravascular LH spaces in these animals. The findings indicated that prolongation of LH infusion did result in progressive flattening of the decay curve after stop-entry. After 1 h of infusion, constant rate infusion/stop-entry decay of LH was nearly as rapid as decay after simple pulse injection of the same extract. After 24 h of infusion, it was nearly as slow as after hypophysectomy/stop-entry. However, this change could not be explained solely on the basis of redistribution, because a similar difference was seen when disappearance of "infused" and "injected" pituitary LH were examined by pulse injection of sera collected from rats which had been given this LH by injection or prolonged infusion. Although variations in extravascular LH "packing" might have influenced LH disappearance in the donor rats, there was no opportunity for such variations to develop in the recipients. Although the mechanism(s) involved in this progressive change in the metabolic clearance characteristics of exogenous (extracted) circulating LH might simply be selective accumulation of the molecules most capable for surviving in the blood, other possibilities exist (e.g. actual mutation of circulating LH molecules). Whether endogenous (secreted) LH undergone similar changes during its sojourn in the circulation is not yet known but these findings suggest that postsecretory mechanisms could contribute to the apparent qualitative difference(s) between stored and circulating rat LH. Several implications of this new information have been discussed.
In both intact and castrated male and female rats, administration of the A-ring reduced androgen, dihydrotestosterone (DHT), consistently failed to stimulate prolactin (PRL) secretion although it inhibited LH release and, in males, stimulated ventral prostate growth. In intact females, but not in the other types of rat, DHT actually suppressed PRL release. These findings do not support generalizations, based entirely on findings with testosterone, that both "androgens" and estrogens exert stimulatory actions on PRL secretion. The distinct stimulatory effects of testosterone and its esters on PRL secretion seem attributable, not to their androgenic actions per se, but to the ability of testosterone to form estrogenic metabolites. This ability does not appear to be shared by the "pure" androgen, DHT.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.