Folia Endocrinologica Japonica
Online ISSN : 2186-506X
Print ISSN : 0029-0661
ISSN-L : 0029-0661
Volume 50, Issue 9
Displaying 1-7 of 7 articles from this issue
  • Takahiko TAKENOUCHI
    1974 Volume 50 Issue 9 Pages 1255-1264,1247
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    The aldosterone secretion rate was measured by radioimmunoassay in regular diets containing approximately 250 mEq of sodium in 12 normal subjects and 47 hypertensive patients. The values ranged from 25.0 to 60.2 ng/day with a mean of 39.6±10.7 (S.D.) in 8 normal males and from 30.2 to 85.4 ng/day with a mean of 62.6±26.8 (S.D.) in 4 normal females. The mean value in 21 cases with benign essentail hypertension was found to be within normal range. No significant difference was found in the aldosterone secretion rate between the gruop of benign essential hypertension with suppressed renin activity and with nonsuppressed renin activity. Metabolic clearance rate in benign essential hypertension was observed to be within normal range. The aldosterone secretion rate in a few cases of benign essential hypertension failed to increase normally in response to sodium restriction (<50 mEq/day). The values in 11 cases of primary aldosteronism were found to be clearly higher, when compared with the values of normal subjects and subjects with benign essential hypertension. High values were found in patients suffering from malignant hypertension and in 3 with unilateral renal artery stenosis. The values in cases of bilateral renal artery stenosis, of pheochromocytoma, and of acromegaly with hypertension were within normal range. Low values in the aldosterone secretion rate were found in 3 cases of 17a-hydroxylase deficiency, and of Cushing's syndrome.
    In summary, the double derivative dilution method for the measurement of the aldosterone secretion rate required both a long period of time as well as complicated technique. The development of radioimmunoassay made it possible to estimate the aldosterone secretion rate easily. Measuring the aldosterone sectreion rate by radioimmunoassay was useful in differentiating primary aldosteronism from benign essential hypertension. z. The difference of the aldosterone secretion rate in response to DOCA was also helpful for the differential diagnosis of primary aldosteronism from benign essential hypertension.
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  • Toshihiro AONO, Masatoshi MIYAZAKI, Junnosuke MINAGAWA, Akira MIYAKE, ...
    1974 Volume 50 Issue 9 Pages 1265-1280,1248
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Serum levels of FSH, LH-HCG and progesterone were determined daily by radioimmunoassay or competitive protein binding assay in 11 cycles from 8 anovulatory patients treated with HMG-HCG or Clomid-HMG-HCG. Hormonal profiles obtained in treated cycles were compared with those of normal cycles.
    The composite hormonal patterns in 6 cycles which resulted in successful ovulation during HMG-HCG therapy were as follows; 1) The mean FSH levels during the follicular phase (17.7 mIU/ml) were higher than that in the normal cycle (7.8 mIU/ml) and no FSH peak was observed around the time of ovulation. 2) No gradual increase of LH was found during the latter half of the follicular phase while LH-HCG peak following HCG injection lasted for 3 days. 3) The mean serum level of progesterone during the luteal phase (19.6 ng/ml) was higher than that of the normal cycle (12.0 ng/ml).
    Two cycles in patients with operated pituitary chromophobe adenoma or Sheehan's syndrome ended in anovulation under HMG-HCG therapy. The basal levels of FSH and LH were low and signs of complete maturation of the ovarian follicle were not achieved.
    In three cycles treated with Clomid-HMG-HCG, the hormonal pattern was similar to that in cycles under HMG-HCG therapy. In addition, an increase of LH during the early follicular and preovulatory phases was obtained.
    In order to simulate hormonal patterns of the normal menstrual cycle under HMG-HCG therapy, the additional use of Clomid during the follicular phase and a single large dose injection of HCG at the time of ovulation are recommended.
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  • Testosterone 17-β-dehydrogenase (NADP) Activity in the Rat Brain and the Effect of Central Acting Drugs upon It
    Takao KANEYUKI
    1974 Volume 50 Issue 9 Pages 1281-1291,1249
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    It has long been a problem how a hormone would affect and be metabolized in the brain. In the present study, Testosterone 17-β-dehydrogenase (NADP) [17-β-Hydroxysteroid 17-β-oxidoreductase (I.I.I.64.)] was found to exist in the mammalian brain. The effect of some central acting drugs on the enzyme was also examined to discover about its relation, if any, to the excitability of CNS.
    1) Identification of Testosterone 17-β-dehydrogenase (NADP) in the mammalian brain.
    4-14C-Testosterone (IμM) was incubated with the supernatant fraction (protein 7.5 mg) of the rat brain homogenate centrifuged at 25,000×g and NADP (60 μM) with the addition of a buffer solution up to the total volume of 10 ml, at 38°C for 120 min. Steroids were extracted with CHCl3 : ether (3 : 1) followed by TLC techniques for separating 4·14C-Δ4-Androstenedione produced, the amount of which was calculated by measuring the radioactivity.
    The properties of the enzyme are as follows; the enzyme has pH optimum of 9.3, it can be inhibited by S-P-CMB, it will catalyze the reversible reaction of Testosterone ⇔Δ4-Androstenedione, and the enzyme activity was found to be higher within a microsomal fraction than in the others.
    2) The enzyme shows a relatively high activity (13 nM/mg protein. 120 min.) in the brain stem of the cat. The enzyme activity of the cat whole brain was about 8 nM/mg protein. 120 min., while the rat whole brain was about 1 nM/mg protein. 120 min.
    3) The effect of some central acting drugs on Testosterone 17-β-dehydrogenase (NADP) activity in the rat brain.
    Rats were divided into 4 groups, each group consisting of ten animals. An individual group was administered intraperitoneally with chlorptomazine hydrochloride (0.4 mg 0.1 ml), diphynylhydantoin sodium (0.5 mg/0.1 ml), imipramine hydrochloride (0.1 mg/ 0.1 ml) or normal saline at the rate of 0.1 ml/100 mg B.W. for 14 days respectively. On the 15th day, the rats were sacrificed by decapitation and immediately the brain was removed, homogenated with 0.32 M sucrose (pH 9.4) and centrifuged at 25,000×g for 15 minutes. The supernatant was used as the source of the enzyme.
    The enzyme activity from the diphenyl hydantoin group (p<0.005) and the chlorpromazine hydrochloride group (p<0.001) was found to increase in comparison with the saline group, while the imipramine hydrochloride group failed to show any significant difference.
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  • Tsuguo UEMURA, Jiro KOOGUCHI, Yoshinori SHIOJIMA
    1974 Volume 50 Issue 9 Pages 1292-1299,1251
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    Synthetic LH releasing hormone (LH-RH) is effecteive in increasing both serum luteinizing hormone (LH) and serum follicle stimulating hormone (FSH) in women with normal menstrual cycle. LH-RH is a substance to use in a test of pituitary function. If serum estradiol (Ed) response to synthetic LH-RH could be evaluated, the function of the hypothalamic pituitary ovarian axis could be clarifed more precisely. Serum levels of LH, FSH and Ed were determined before and after intramuscular administration of 100 /2g LH-RH in 36 anovulatory women.
    LH and FSH levels in the serum were measured by the double antibody method of radioimmunoassay. Ed levels were determined by the radioimmunoassay method of T. Makino, using the antiserum against Ed-6-BSA donated by Dr. T. Makino and applying microcolumn of sephadex LH 20.
    Study of the LH secretion led to the delineation of three types of pateint.
    Type 1 patients showed high basal LH levels exceeding 50 mIU/ml and well response to the LH-RH. (ovarian lesion type)
    Type 2 patients showed low basal LH levels and poor response to the LH-RH. (pituitary lesion type)
    Type 3 patients showed low basal LH levels and well repsonse, the increment being over two-fold. (hypothalamic lesion type)
    Serum levels of Ed before and after administration of LH-RH in these types of patients were as follows.
    Type 1 and Type 2 patients had low initial levels of serum Ed under 30 pg/ml. There was an inconsistent response to the LH-RH.
    Type 3 patients were divided into 3 groups by study of the Ed secretion.
    1) Low basal Ed levels and poor Ed responses (serious grade)
    2) High basal Ed levels and poor Ed responses (moderate grade)
    3) High basal Ed levels and well Ed responses (mild grade)
    Patients with anovulatory cycle and patients with 1st grade amenorrhea showed mild, moderate or serious hypothalamus disturbance, and patients with 2nd grade amenorrhea had a disturbance in the ovary, piruitary or hypothalamus (serious grade or moderate grade).
    These present data demonstrate the usefullness of the “dynamic LH-RH test” to facilitate the exact diagnosis of endocrine disturbances in anovulatory women.
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  • Norio OGAWA, Masanori MIYOSHI, Shinya SUZUKI, Tadashi OFUJI, Katsushi ...
    1974 Volume 50 Issue 9 Pages 1300-1309,1252
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    A sensitive radioimmunoassay (RIA) for human prolactin (hPRL) was developed with purified hPRL and antiserum to hPRL (kindly supplied by NIAMDD, U.S.A.). HPRL was iodinated by a modification of the enzymatic method of Miyachi et al. (1972) using lactoperoxidase. When the radioiodinated hPRL was passed through a 1.5 × 50cm column of Sephadex G-100, it usually separated into three peaks. By the solid-phase RIA using antibody-coated plastic disposable microtiter trays, it was confirmed that the second peak consisted of the immunoreactive material that was used for RIA. For the measurement of plasma hPRL levels, the double antibody technique was used to separate bound from free labeled hormones. The average coefficients of variation were 11.7% in within assays and 14.8% in between assays.
    Basal plasma hPRL levels in normal subjects were less than 20 ng/ml. The mean basal hPRL levels were 10.2 ±4.9 (Mean±SD) ng/ml in 13 normal men and 9.6±5.4 ng/ml in 8 normal women; no statistically significant sex difference was observed.
    When synthetic TRH (TANABE SEIYAKU Co., LTD) was administered intravenously to a normal male subject, the maximum increase in plasma hPRL above the baseline level increased lineally as a function of the log of the TRH dose between 25 and 100 /2g of TRH. Intravenous administration of 500, μg of TRH caused a significant increase in plasma hPRL in all of the 10 normal subjects tested, and the peaks were observed 15 or 30 minutes after the injection.
    Plasma hPRL levels in 2 patients with Sheehan's syndrome and in a patient with operated-irradiated chromophobe adenoma tended to be low, and they showed no significant increase in plasma hPRL after TRH injection. Basal plasma hPRL levels in most of the patients with hypothalamo-pituitary tumor tended to be high. Especially marked elevated plasma hPRL levels were observed in a patient with chromophobe adenoma, in a patient with ectopic pinealoma and in an operated craniopharingioma, while 3 patients with diabetes insipidus showed normal hPRL levels. Plasma hPRL levels were normal in most patients with pituitary dwarfism.
    Plasma hPRL levels in 2 patients with hyperthyroidism tended to be low, and they showed no significant hPRL response to TRH, while patients with hypothyroidism showed normal or rather exaggerated hPRL response to TRH.
    Plasma hPRL levels were normal in most of the patients with Cushing's syndrome and plasma hPRL repsonses to TRH in these patients were normal. Two out of 7 patients with Cushing's syndrome showed slightly elevated basal plasma hPRL levels with slightly impaired response to TRH, while patients with operated Cushing's syndrome showed normal basal plasma hPRL levels with normal response to TRH.
    TRH-induced hPRL secretion tended to be impaired in patients receiving long-term and high doses of glucocorticoid.
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  • Yuzo OHGA
    1974 Volume 50 Issue 9 Pages 1310-1322,1254
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
    The effects of placental peptide hormones (hCS, human chorionic somatomammotropin, and hCG, human chorionic gonadotropin) on the adenyl cyclase-cyclic AMP-protein kinase system in their target organs were studied.
    The extraction method of cyclic AMP was also evaluated. The cyclic AMP level measured by Gilman's method using rat liver cyclic AMP binding protein was affected by the extraction method of cyclic AMP from the tissue and the volume of the starting material. When there was enough material, Dowex 50, H+ form column chromatography was effective for the extraction of cyclic AMP from tissue. But when there was only 50 mg of material or less, it was necessary that cyclic AMP be extracted from tissue by 6% trichroloacetic acid only many samples were assayed in order to reduce error.
    On the cyclic AMP binding assay itself, it was necessary to fix the time between the end of the reaction and filtering with millipore filter.
    The lipolytic action of hCS was studied in rat epididymal fat pads. The level of cyclic AMP was elevated in rat epididymal fat pads in vitro and in vivo by hCS. The protein kinase activity was also increased in rat epididymal fat pads in vitro experiment by hCS. Furthermore, hCS caused an increase in the FFA level in the incubation medium in vitro and in the serum.
    These results indicated that hCS acted in the lipolysis in the rat via the adenyl cyclase-cyclic AMP-protein kinase system.
    The effect of hCG on the protein kinase activity in rat ovary was studied.
    The protein kinase activity was increased in the ovary of normal cycle rats, pregnant rats, and premature rats in vitro by hCG. This result suggested that the effect of hCG on the rat ovary was accomplished via the adenyl cyclase-cyclic AMP-protein kinase system.
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  • 1974 Volume 50 Issue 9 Pages 1323-1340
    Published: September 20, 1974
    Released on J-STAGE: September 24, 2012
    JOURNAL FREE ACCESS
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