The role of sex steroids in the programming of the level of serum corticosteroid-binding globulin (CBG) in the rat has been studied at different stages of ontogenesis. The CBG content in the serum of mature female rats was 2.5 times higher than that in male rats. Sexual dimorphism of CBG content was absent in immature animals of 3-4 weeks of age. Castration of mature rats led to a 40-50% increase in CBG content. The CBG concentration in mature females or castrated adult males treated with testosterone propionate (TP; 3 mg/day for 4 days) was decreased by 40-50% compared with vehicle-treated rats. Oestradiol injection (1 microgram/day for 4 days) had no influence on CBG levels in mature male and ovariectomized adult female rats. Immature rats were castrated on days 1, 7, 14, 21, 28 or 35 of age and the CBG level was determined at 10-12 weeks of age. The CBG content of rats castrated up to day 28 of age was 2.5 times higher than that in mature males and did not differ from that in mature females. The CBG content of male rats castrated on day 35 of age was the same as that of adult castrated males. The CBG level in castrated rats treated with TP (1.25 mg for days 1-3 or 300 micrograms/day for 5 days after castration at day 7 up to day 26) did not differ from that in controls (i.e. vehicle-treated rats).(ABSTRACT TRUNCATED AT 250 WORDS)

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The use of a modified, adequate method of quantification of estrogen receptors has permitted us to prove the existence of sex-specific peculiarities in rat liver estrogen reception and their significance for the realization of sex-dependent changes in angiotensinogen plasma level after estrogenization. Endocrine mechanisms for the formation of sex-related differences in hepatic estrogen receptor content in rats were investigated in detail. The investigation shows that androgens have negative regulatory influence on the hepatic estrogen receptor level in rats. Estrogens and adrenal and thyroid hormones do not take part in the regulation of hepatic estrogen receptor content in rats. It has been proven that the decisive role in keeping up a certain estrogen receptor concentration in hepatocytes belongs to pituitary growth hormone. It was shown for the first time that androgens are able to inhibit the stimulatory effect of growth hormone on hepatic estrogen receptors.