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NOTES AND COMMENTS 421 first large increase in ovarian weight was not found until 96 hr. Ovary weight remained high at 108 and 120 hr but declined at 132 hr. It was again up at 144 hr, but in this group the large variability casts doubt on the significance of the increase. There is the possibility that all the animals were not phase synchronized in their FSH output: In 2 of 6 animals ovaries were control size but in 2 they were above 70 mg. With the assay system used, increases in endogenous FSH above that in normal controls are difficult to demonstrate as the animals get older.Considering the present results it is difficult to conclude that progesterone prevents testosterone-induced precocious puberty by inhibiting the FSH-stimulating action of the androgen. Essentially the full effect of androgen on FSH output was accomplished, only slightly delayed. On the other hand, progesterone could very well inhibit the action of estrogen in inducing precocious puberty by inhibiting its action on FSH-controlling mechanisms.ABSTRACT. Effects of androgens on the hypocalcemic response of rats to porcine thyrocalcitonin were examined. Thyrocalcitonin (0.02 0.08 MRC U) administered sc induced 60 min thereafter a more pronounced hypocalcemia in the male sham-operated than in the male castrated animals. In the male, the hypocalcemic response was markedly enhanced by prior treatment with testosterone propionate (0.1~1.0 mg) for 3 days. The same treatments provoked lesser changes of similar type in the female spayed as well as in the female sham-operated animals. Endogenous androgens and exogenous testosterone propionate caused inconsistent alterations in the basal levels of serum calcium and phosphate. The sensitization of animals to thyrocalcitonin could not be accounted for by their effects on serum phosphate concentration. {Endocrinology 87: 421, 1970)

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SynopsisThe hypocalcemic response in rabbits to parotin (a protein fraction from the bovine parotid gland) was studied in detail. Intravenous parotin produced a significant hypocalcemia appearing at 2hr, peaking at 4hr, and returning to the control at 10hr, after the dosage. The hypocalcemia was distinct in the time course from that induced by thyrocalcitonin or adrenocorticotropin; the latter hormones produced a significant hypocalcemia within 30min. The evidence was also presented that the parotin effect was neither a consequence of the induced secretion of thyrocalcitonin or adrenocrticotropin, nor that of the suppressed secretion of parathyroid hormone. As judged from the per cent decrease, the extent of hypocalcemia was similar whether the serum calcium was assessed by the assay of total calcium or by the assay of titratable calcium. By contrast, the serum ionic calcium was apparently not influenced by the parotin administration. These results suggest that parotin acts in rabbits, largely independently of the parathyroid and calcitonin system, to cause a decline in the level of serum calcium binding capacity.