The effect of ketoconazole on steroid synthesis was studied in intact (sham-operated) and castrated male and ovariectomized female rats. Rats were given 25 mg/kg ketoconazole twice a day im for 5 days. The influence of ketoconazole was also investigated on hormone release altered by GnRH, estradiol and haloperidol. The following hormones were measured: serum LH, PRL, testosterone, corticosterone, 17-OH-progesterone, estradiol, and dopamine content of the tubero-infundibular area. Ketoconazole treatment resulted in a significant decrease of testerone level (from 7.93 \m=+-\1.99 to 3.83 \m=+-\0.94 nmol/l), whereas LH, PRL, corticosterone and 17-OH\x=req-\ progesterone remained unchanged in the male rat. The effect of castration on LH level was reduced by ketoconazole in male (from 590 \m=+-\35 to 390 \m=+-\25 \g=m\g/l ) and female rats (from 468 \m=+-\22 to 346 \m=+-\39 \g=m\g/l ), but the GnRH-stimulated LH release in castrated and ovariectomized animals was unchanged. The suppressive action of estradiol on LH in ovariectomized rats was enhanced (from 160 \ m=+-\41 to 64.6 \m=+-\12.9 \g=m\g/l ),and its priming effect on PRL release was diminished by ketoconazole (from 598 \ m=+-\ 81 to 281 \ m=+-\ 66 \g=m\g/l ). Ketoconazole failed to modify the tubero-infundibular dopamine content and haloperidol-induced PRL release. It can be assumed that in addition to its inhibitory role of steroid biosynthesis ketoconazole has an influence on central mechanisms underlying LH and PRL release. Ketoconazole (KZ) is an äntifungal agent with a marked effect on steroidogenesis in humans and in animals, inhibiting the enzyme activity of the cho¬ lesterol side-chain cleavage enzyme, 17-hydroxylase, 11-hydroxylase, and mostly the 17-20-desmolase activity (1-6). Schurmeyer & Nieschlag (7) suggested that a phenylated side chain of the imidazole molecule is responsible for the inhibition of testosterone biosynthesis. Some data show that the substance is able to reduce ovarian aromatase ac¬ tivity in the rat (8,9). Basal aldosterone and cortisol levels are not necessarily altered by KZ, presumably because the inhibitory process is partial, and can be unequivocally demonstrated when the synthesis of these steroids is stimulated (10-13). The androgen steroid production is more sensitive to KZ suppres¬ sion, and with long-term treatment a 50 per cent decrease of testosterone level can be achieved (14,15). According to Santen et al. (16) and Bhasin et al. (17) the low serum testosterone concentrations were not accompanied by the expected rate of in¬ crease in LH and FSH release. It was assumed that KZ might have a direct effect at the pituitary level, but this has not been confirmed on castrated male rats (17). The present work was devoted to studying the actions of KZ on hypothalamic and pituitary mech¬ anisms in the rats, and to investigating the suppressive effect of the drug on the stimulated LH release in vivo. Materials and MethodsAnimals and treatment protocol Adult male and regularly cycling female rats of the Wistar strain were used....

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(a) there is no close correlation between the hormone granules detected in the pituitary adenoma cells - by light microscopic, immunocytochemical and electron microscopic methods - and the serum hormone levels, their response to TRH; (b) in hormonally active adenomas the immunocytochemical as well as the ultrastructural findings could be negative; (c) in one disease more hormones could give an immunopositive reaction; (d) in any types of investigated adenomas the TSH immunopositivity was always accompanied by PRL immunopositivity (6 cases); (e) the size and the clinical (serum) or cytological hormone activity of the adenomas were independent of one another; (f) the basal serum hormone level shows the hormonal activity of the pituitary adenoma best of all.

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Effects of a 72-h prostacyclin (PGI2) infusion (5 ng/kg/min) on hormone levels were studied in 11 patients (5 males, 6 females) suffering from obliterative arterial disease of the lower extremities. ACTH, cortisol, TSH, prolactin (Prl), GH, LH, FSH, T3, T4, calcitonin, parathyroid hormone (PTH), insulin, plasma renin activity (PRA), aldosterone and testosterone levels were measured at \m=-\15, 0,30, 120, 240 min and 24, 48, 72 and 96 h after the infusion. During the first 240 min Prl and GH levels showed an increase that was thought to be either an effect of release of hormones or a consequence of stress. At the same time the thyroid hormones, T3, T4 and calcitonin decreased, presumably owing to an alteration in the blood flow to the thyroid gland. All these hormone levels returned to normal at 24 h in spite of the infusion continuing. PRA increased only during the second half of the infusion. No changes were found in the levels of ACTH, cortisol, TSH, LH, FSH, PTH, insulin, aldosterone and testosterone during the infusion. Five diabetics showed the same hormonal changes as the non-diabetics and their blood sugar levels remained unaffected during and after the procedure.