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Oestradiol-17\g=b\,diethylstilboestrol (DES), dl-dihydrodibutylstilboestrol (dl-DHBS) and meso-dihydrodibutylstilboestrol (meso-DHBS) were injected intramuscularly into male Sprague-Dawley rats in a daily dose of 100 \ g=m\ g for a period of 10 days. Oestradiol-17\g=b\ and DES decreased the weight of the prostate and seminal vesicles to the same extent, whereas meso\x=req-\ DHBS was less effective. dl-DHBS was almost inactive. Only oestradiol\x=req-\ 17\g=b\ and DES caused a decrease in the weight of the testes. The adrenal glands increased in weight after administration of either oestradiol-17\g=b\, DES or meso-DHBS.Four hormones in the plasma were measured: testosterone, androstenedi\x=req-\ one, prolactin and interstitial cell-stimulating hormone (ICSH). DES decreased the plasma concentration of both ICSH and testosterone. Oestradiol-17\g=b\ and meso-DHBS administration resulted in a lowering of the plasma testosterone concentration with no effect on ICSH. Oestradiol-17\g=b\, DES and meso-DHBS markedly increased plasma prolactin concentrations. dl-DHBS appeared to have little biological effect causing only very small changes in all the parameters investigated.

SummaryPlasma prolactin has been estimated in 69 psychiatric in-patients receiving either thioridazine (20–300 mg./day) or chlorpromazine (50–200 mg./day) or other phenothiazines. A homologous radioimmuno-assay was used which depends on an antiserum to human amniotic prolactin. Prolactin levels were significantly increased in these patients compared with control patients, and were dose related. Simultaneous estimation of growth hormone revealed normal levels.

SUMMARY Plasma prolactin and thyrotrophin (TSH) were measured by radioimmunoassay before, at 20 min and 60 min after the intravenous administration of 200 μg thyrotrophin‐releasing hormone (TRH) in thirty‐two patients with untreated primary hypothyroidism and in sixteen normal volunteers. Whereas basal plasma TSH was markedly elevated in all the patients with hypothyroidism, a slight, but significant increase (P<0.05) in basal plasma prolactin in primary hypothyroidism could only be demonstrated by matching for age, sex and circulating gonadotrophin levels, ten patients with hypothyroidism with ten normal volunteers. There was, however, no significant difference between the two groups, matched or unmatched, in the plasma prolactin levels, in contrast to the plasma TSH levels, following TRH administration. No apparent relationship was found between basal prolactin and follicle‐stimulating hormone (FSH), luteinizing hormone (LH) or TSH. Assuming the release of prolactin by TRH to be of physiological significance, the results suggest that TRH secretion by the hypothalamus may be increased in untreated hypothyroidism and that low levels of circulating thyroid hormone increase the sensitivity of the pituitary thyrotrophs, but not the prolactin secreting cells, to TRH. Markedly elevated plasma prolactin levels associated with galactorrhoea were not seen in primary hypothyroidism in the absence of the puerperium or oestrogen therapy.