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53 巻, 3 号
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荻原 俊男, 市原 清志, 熊原 雄一, 山本 智英, Henry W. Kircher, Charles A. Nugent1977 年 53 巻 3 号 p. 175-182
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーThe mineralocorticoid activities and effects on blood pressure of synthetic 16 (βdihydroxy-5-androsten-17-one) and its isomer, 16-oxo-A (16-oxo-androstenediol, 3β, 17β- dihydroxy-5-androsten-16-one) were examined in rats. In study 1, three groups of 5 rats each were given subcutaneous injections of 0.2 ml of ethanolic solutions for 4 weeks. Their drinking water contained 1% NaCl. In group I, the control group, 20% ethanol was injected.Each rat at in group II was given a daily injection of 20% ethanol containing 400pg of 16β- OH-DHEA. Each rat in group III was given a daily injection of 400 μg of 16-oxo-A in 20% ethanol. Body weight and systolic blood pressure were monitored twice weekly. The urinary Na+/K+ ratio was determined on the 14th and 29th days. Serum Na+, K+, and hematocrit analyses were done on the 29th day. Plasma renin activity was assayed in samples obtained before and after furosemide administration on the 29th and 30th days, respectively. There were no significant differences in the mean values of any of the determinations listed above between groups II and III (treated) and group I (control) with one exception. The mean hematocrit of group II was slightly (4%) but significantly (P<0.01) less than that of the control group on the 29th day.
In study 2, unilaterally nephrectomized salt loaded male Wistar rats were injected once a week with large doses of steroids in sesame oil for 2 month periods. Rats injected with 10 mg and with 30 mg of 11-desoxycorticosterone acetate per kg of body weight per week developed hyertension. Rats given 30 mg/kg BW/week of 16β-OH-DHEA or 16-oxo-A and control rats did not develop hypertension.
Other investigators have postulated that 16β-OH-DHEA and possibly its 16-oxo isomer are direct causative factors in the pathogenesis of low renin hypertension in humans. In contrast, we have not been able to demonstrate any substantial minerolocorticoid activity or any effect on blood pressure for either of these steroids. We conclude that it is unlikely that 16β-OH-DHEA and 16-oxo-A are direct causative factors in the production of low renin essential hypertension. On the other hand, if 16β-OH-DHEA is excreted in abnormally large amounts in the urine of patients with low renin hypertension, it may be a maker of the disease even if it is not a direct causative factor.抄録全体を表示PDF形式でダウンロード (632K) -
斎田 幸次, 中村 章, 金沢 精一, 足高 善彦, 望月 真人, 東條 伸平1977 年 53 巻 3 号 p. 183-195
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーIt is well known that a thyroid stimulator, human chorionic thyrotropin (hCT), as well as human chorionic gonadotropin is secreted from normal placental tissue.
After extraction of thyrotropic and gonadotropic activities from placental powder by percolation with solutions of decreasing ethanol content, the concentrate was chromatographed on carboxymethyl cellulose (CM-cellulose) with subsequent gelfiltration of the active fractions on Sephadex G-100 and chromatography on DEAE-cellulose and DEAE-Sephadex A-50.
Thyrotropic and gonadotropic activities were isolated by the procedures used in our laboratory. The steps in chromatography on CM-cellulose and DEAE-Sephadex A-50 used are important for the isolation of hCG from hCT. The potencies of the final products were 250 mU/mg of hCT and 8,200 IU/mg of hCG.
Commercial hCG of urinary origin (12,000 IU/mg) was purified by a similar method of chromatography on CM-cellulose. The bulk of hCG was localized in the unadsorbed fraction (14,000 IU/mg) with conductivity of 0.5 m mho, pH 6.0 NH4Ac, and thyrotropic activity in the adsorbed fraction was eluted between conductivities of 5.2 -11.3 m mho.
These results indicated that the chromatographic properties were different between hCT and hCG.
On the other hand, the authors examined the effect of varying concentration of hCT and hCG on cyclic AMP levels in a guinea pig thyroid slice.
An increase in the level of cyclic AMP has been observed in response to hCT, but hCG had no effect on the level of cyclic AMP in guinea pig thyroid slices.
Recently, the question had been raised as to whether the thyroid stimulator found in the serum and tumor of patients with trophoblastic disease and hyperthyroidism might be hCG. The present results, however, strongly suggest that hCG is not thought to be the thyroid stimulator which has been found in normal placenta.抄録全体を表示PDF形式でダウンロード (1024K) -
-アンギオテンシンII・ACTH2重負荷刺激におけるアルドステロン分泌動態-畑 俊一, 国田 晴彦, 吉岡 光明, 岡本 正敏1977 年 53 巻 3 号 p. 196-202
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーIt is well known that the regulation of aldosterone secretion is governed by the reninangiotensin system, ACTH and electrolytes (Na and K) in plasma. However, the relationships between these regulating factors of aldosterone secretion still remain unclear. In order to study the relationships between these regulating factors of aldosterone, we examined the effects of angiotensin II plus ACTH under various conditions on plasma aldosterone in normal subjects.
Men aged 19-23 years were selected for testing. Using 4 groups, containing 5 men each, the following experiment was performed. Group I : Angiotensin II (5 ng/kg/min.) was infused at 1800 hours. Group II : β1-24 ACTH (0.25 mg) was injected intravenously at 1800 hours. Group III : Infusion of angiotension II and injection of ACTH were performed at 1800 hours. Group IV : Infusion of angiotensin II was performed at 1700 hours and injection of ACTH was performed at 1800 hours.
In Group I, plasma aldosterone increased with maximum peak attained 60 minutes after infusion of angiotensin II. In Group II, plasma aldosterone increased with maximum peak attained 60 minutes after injection of ACTH. In Group III, plasma aldosterone increased after infusion of angiotensin II plus injection of ACTH more significantly than after infusion of angiotensin II or injection of ACTH. In Group IV, plasma aldosterone increased after infusion of angiotensin II and continuously increased after injection of ACTH.
From these results, we concluded that infusion of angiotensin II and injection of ACTH at the same time cause additional increase in plasma aldosterone, and that not only preceding stimulation (angiotensin II), but also following stimulation (ACTH) cause an increase in plasma aldosterone.抄録全体を表示PDF形式でダウンロード (492K) -
宮本 紀男1977 年 53 巻 3 号 p. 203-220
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーPlasma progesterone (P), 17α-OH-progesterone (17P), estrone (E11), 17β-estradiol (E2), estriol (E3) and hCG were measured simultaneously with competitive protein binding assay or radioimmunoassay. Thirty-one patients with trophoblastic diseases including twenty-one hydatidiform moles, two destructive moles, four chorioepitheliomas and four unestablished trophoblastic diseases were studied. Blood samples of these subjects were taken serially before, during and after treatments. The mean concentration of P in cases of unaborted hydatidiform moles was 40.0 ± 13.7 ng/ml (Mean ± S.D.) and those of 17P, E1 and E2 were 4.90 ± 6.08, 0.71 ± 0.92 ng/ml and 2.30 ± 2.55 ng/ml respectively. Plasma 17P in cases of unaborted hydatidiform moles was significantly higher than those of normal pregnancies corresponding to gestation weeks, but the other steroids were not so high in comparison with normal pregnancy. E3 values were not detectable in all patients studied even after the 15th week of gestation.
In cases of destructive moles, the mean concentration of P was 31.5 ± 0.71 ng/ml corresponding with 10th week of gestation, and the other steroids were rather low. Most of the patients with chorioepithlioma and unestablished trophoblastic disease showed low steroid levels. Although there was some correlation among each steroid level, there was no correlation between hCG and each steroid in trophoblastic diseases.
The levels of plasma steroids fell rapidly preceding the decrease in plasma hCG after the evacuation of hydatidiform moles. In the cases which developed to destructive moles, P, 17P and E2 elevated together with hCG again and then fell rapidly after the hystrectomy. Daily fluctuation of each steroid was not recognized in a chorioepithelioma.抄録全体を表示PDF形式でダウンロード (1553K) -
内海 正文, 棋村 博之, 佐古田 雅弘, 馬場 茂明1977 年 53 巻 3 号 p. 221-234
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーFundamental study of a radioimmunoassay for somatostatin (growth hormone release inhibiting factor : GIF or GHRIF) is described in detail.
The antiserum to somatostatin was generated by immunizing rabbits with somatostatin conjugated human serum globulin.
Tyr1 -somatostatin was radioiodinated by the method of Hunter and Greenwood with the modification using bovine serum albumin (BSA), without sodium metabisulfite to avoid reduction of the disulfide bond and then the labelled hormone was separated from 125I-BSA and free 125I by passage through a column (0.8 X15 cm) packed with Sephadex G-25. The column was equilibrated and eluted with 0.1 N acetic acid, pH 3.0, containing 0.25% BSA. The elution pattern of radioactivity revealed three peaks. The first and the second peak contained 125I-BSA and free 125I respectively. Labelled tyr1 -somatostatin was absorbed to Sephadex G-25 and eluted broadly after free 125I (the third peak). An antiserm at final dilution of 1 : 4000 bound 35% of this labelled hormone. However, the labelled hormone was damaged progressively even when stored at -20°C in 0.1N acetic acid, pH 3.0.
The separation of the free and the bound hormone was performed by double antibody method.
Based on the results of studies of assay's conditions (buffer composition, antibody concentration, incubation time, incubation temperature), the assay was carried out as follows :
To each reaction tube 0.5 ml diluent buffer (0.01 M phosphate buffer, 0.15 M NaCl, pH 7.6, containing 1% BSA), 0.1 ml standard somatostatin or samples to be tested, 0.1 ml 125I tyr1-somatostatin (approximately 10000 cpm), 0.1 ml anti-somatostatin serum (diluted 1 : 500) were mixed. After the first incubation at 4°C for 4 days, 0.1 ml anti-rabbit-γ-globulin goat serum (diluted 1 : 20) and 0.1 ml normal rabbit serum (1%) were added. After thd second incubation at 4°C for 1 or 2 days, the assay tubes were centrifuged at 3000 rpm for 30 minutes and the precipitates were counted.
Various synthetic hypothalamic, highly purified hypophysiotropic and pancreatic hormones did not interfere with the radioimmunoassay for somatostatin.
A dose-response curve was obtained in a range from 7.8 pg to 500 pg per tube of standard somatostatin in this assay system. A dilution curve of rat hypothalamic extract paralleled that of standard somatostatin. Intra-assay coefficient of variation was 4.92%.
These results of radioimmunoassay for somatostatin indicate that the assay system is sensitive and fairly specific and useful to investigate the physiological roles of somatostatin on the regulatory mechanism of various hormones and enzymes.抄録全体を表示PDF形式でダウンロード (1173K) -
野々田 昶1977 年 53 巻 3 号 p. 235-249
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーResponses of the hypothalamic-pituitary-adrenal axis to the administration of glucocorticoids were investigated in infants and children, particularly with respect to development of those responses. The group of subjects consisted of 57 individuals. One portion contained 36 persons ranging in age from three months to 15 years who had no endocrine or central nervous system disorders. Six adults in good health comprised another portion. These subjects were separated into the following four groups : infants of three months to one year; younger children of one to six years; older children of seven to 15 years; and adults or those 20 to 30 years old. Finally, 15 patients with congenital adrenal hyperplasia, primordial dwarfism, central nervous system disorders or anorexia nervosa were studied.
Serum cortisol levels were determined from blood samples taken at 9 a.m. for 3 consecutive days both before and after the intramuscular injection of dexamethasone at 11 p.m. The method of measurement followed the competitive protein-binding technique of Murphy. For purposes of comparison, the measured serum cortisol levels were transformed into suppression rates from results obtained before and after the administration of dexamethasone.
No significant differences of suppression rates were found among these four age groups when dexamethasone was given according to body surface area (0.25 mg/m2). It was noted in infants that with increasing doses of dexamethasone (0.06 mg -0.50 mg/ m2), the suppression rates likewise increased. Suppression rates of subjects with anorexia nervosa, however, were abnormally low. These results indicate that infants and children have a negative feedback mechanism operating on the hypothalamic-pituitary-adrenal axis of approximately the same level observed in adults. Negative feedback mechanism may be affected in some diseases, for example anorexia nervosa.抄録全体を表示PDF形式でダウンロード (1113K) -
山田 律爾, 中井 利昭1977 年 53 巻 3 号 p. 250-258
発行日: 1977/03/20
公開日: 2012/09/24
ジャーナル フリーThe effect of phentolamine (regitine) on the in vitro release of catecholamines from adrenal medulla has been studied.
Firstly, a continuous flow incubation (perifusion) system was developed in which secretory responses of adrenal medulla to acetylcholine were characterized by serial fluorimetric assay of catecholamine in the effluent medium. There was an initial massive release of catecholamine, which in the absence of acetylcholine, declined to a low basal level. The basal level was stable. Following 2.5 h preincubation, catecholamine release rose abruptly after addition of 10-2M acetylcholine to the medium and returned promptly to baseline after withdrawal. Pretreatment of pig adrenal medulla with 10-2M phentalamine blocked the increase of catecholamine overflow by 10-2M acetylcholine. It was also found that phentolamine, itself, caused no effect on catecholamine release from adrenal medulla.
These results show that phentolamine blocked the catecholamine release from perifused pig adrenal medulla in response to acetylcholine infusion.抄録全体を表示PDF形式でダウンロード (704K)
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