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62 巻, 7 号
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副腎皮質各種ステロイドのアンジオテンシンIIまたはACTHに対する反応性によるアルドステロン生合成過程の検討柳沼 健之1986 年 62 巻 7 号 p. 755-775
発行日: 1986/07/20
公開日: 2012/09/24
ジャーナル フリーThis study was designed to clarify the cause of hyporeninemic hypoaldosteronism (HH) associated with diabetes mellitus. Fourty diabetic patients (DP) were divided into 3 groups; 12 patients without neuropathy or nephropathy, 13 with neuropathy and without nephropathy, and 15 with neuropathy and nephropathy; in the third group 3 HH patients were included. Fourteen normal subjects served as controls. In all DP and the normal sub(PAld), jects, plasma concentration of aldosterone 18-hydroxycorticosterone (P18-0H-B), corticosterone (PB), 11-deoxycorticosterone (PDOC) and cortisol (PF) were measured before and after intravenous administration of angiotensin II (A II, 10 ng/kg/min, for 30 min) or ACTH (1-24 ACTH, 0.25 mg). In 27 DP, plasma renin activity (PRA) increased from 0.8 ±0.6 SD to 2.4 ±2.2 ng/ml/h (normal : 1.2 ±0.7 to 3.2 ±1.7 ng/ml/h) 2 hours after intravenous administration of furosemide (1 mg/kg) and assumption of the upright posture. No significant difference in PRA was found between DP and controls, whereas the response to these stimuli decreased significantly in 9 DP with neuropathy and nephropathy (from 0.4 ±0.2 to 0.7 ±0.4 ng/ml/h). The major results were as follows :
1) The mean of PAld (5.9±2.4 ng/100 ml) in DP was significantly lower than that in controls (7.7 ±2.2 ng/100 ml). There was no significant difference of P Ald between DP without complications and controls. PAld in DP with neuropathy alone (5.0 ±1.5 ng/100 ml, p<0.05) and that in DP with neuropathy and nephropathy (4.7 ±2.4 ng/100 ml, p<0.05) were lower than that in controls. The mean of P18-0H-B (12.3 ±4.3 ng/100 ml) in DP was similar to that (14.2 ±3.2 ng/100 ml) in controls. P18-0H-B in DP without complications and that in DP with neuropathy alone were similar to that in controls. However, P18-OH-B (8.8 ± 3.2 ng/100 ml) in DP with neuropathy and nephropathy was significantly lower than that in controls (p<0.001). No difference in PB, PDOC or PF was observed between DP and controls.
2) PAld increased from 6.0 ± 2.5 ng/100 ml in DP (p<0.001) and from 7.6 ± 2.2 to 15.7 ± 5.3 ng/100 ml in controls (p<0.001) 30 min after A II infusion. PAld increased from 7.6 ± 2.5 ng/100 ml in DP without complications (p<0.001), from 5.9 ± 1.5 ng/100 ml to 7.0 ± 1.8 ng/100 ml in DP with neuropathy alone (p<0.001) and from 4.7 ± 2.4 ng/100 ml to 5.5 ± 2.5 ng/100 ml in DP with neuropathy and nephropathy (p<0.01). The increments in the 3 groups were significantly lower than that in controls (p<0.05, p<0.001, p<0.001). P18-0H-B increased from 12.1 ± 4.5 to 15.4 ± 6.8 ng/100 ml in DP (p<0.001) and from 14.1 ± 3.5 to 26.6 ± 5.0 ng/100 ml in controls (p<0.001) after A II infusion. P18-0H-B increased from 15.3 ± 4.2 to 22.3 ± 7.3 ng/100 ml in DP without complications (p<0.001), from 13.1 ± 2.8 to 14.7 ± 2.9 ng/100 ml in DP with neuropathy alone (p<0.001) and from 8.7 ± 3.7 to 10.6 ± 3.5 ng/100 ml in DP with neuropathy and nephropathy (p<0.01). The increments of P18-0H-B in DP with neuropathy alone (p<0.001) and in DP with neuropathy and nephropathy (p<0.001) were lower than that in controls. PB, BDoc and PF did not change significantly after A II infusion in either controls and DP.
3) PAld increased from 6.0 ± 2.3 to 16.2 ± 7.2 ng/100 ml in DP (p<0.001) and from 7.6 ± 2.2 to 24.6 ± 5.3 ng/100 ml in controls (p<0.001) 60 min after ACTH administration.抄録全体を表示PDF形式でダウンロード (2328K) -
重富 秀一, 上野 修一, 戸崎 英夫, 鴻野 浩, 橋本 重厚, 福地 総逸1986 年 62 巻 7 号 p. 776-783
発行日: 1986/07/20
公開日: 2012/09/24
ジャーナル フリーWe investigated the effects of short-term and long-term sodium loading on the sympathoadrenomedulary system and renal dopamine receptor. Male Wistar rats (n=30) were raised drinking 1% NaCl for four weeks. Urinary norepinephrine and epinephrine excretion (UNE and UE) were measured before and 1, 2, 4 weeks after sodium loading by the use of high pressure liquid chromatography with fluorescence spectrophotometer. Renal plasma membranes were prepared by the ultracentrifugation method, and maximal binding capacity (Bmax) and dissociation constant (Kd) of renal dopamine receptor were determined by Scatchard analysis using 3-H-spiperone.
Results : Sodium loading caused a slight but not significant decrease of free UNE after 1 and 2 weeks then clear increments of total (free + conjugated) UNE, free UE and total UE after 4 weeks. Bmax of renal dopamine receptor did not change after 1 and 2 weeks but significantly decreased after 4 weeks (before : 535.9 fmol/mg·protein, after 4 weeks : 327.2 fmol/mg·protein). Kd of renal dopamine receptor slightly elevated 1 week after sodium loading and then returned to the initial level.
Conclusion : These data suggest that short-term sodium loading may suppress the sympathetic activity, but long-term sodium loading may increase the activity of the sympathoadrenomedullary system with the decrease of renal dopamine receptor concentration. Increased catecholamines and decreased renal dopamine after long-term sodium loading may contribute to sodium-dependent hypertension.抄録全体を表示PDF形式でダウンロード (691K) -
第一編正常妊娠時におけるカルシウム代謝とカルシウム調節ホルモンの分泌動態小原 範之, 森川 肇, 上田 康夫, 望月 眞人1986 年 62 巻 7 号 p. 784-796
発行日: 1986/07/20
公開日: 2012/09/24
ジャーナル フリーDynamic changes in maternal and fetal calcium metabolism during pregnancy were investigated by simultaneously measuring serum or urinary concentrations of calcium and calcium regulating hormones.
Serum concentrations of total calcium in maternal serum decreased significantly, but those of ionized calcium decreased slightly but not significantly late in pregnancy. Maternal serum levels of parathyroid hormone (PTH) were almost the same as non-pregnant values throughout pregnancy, but those of 1α, 25-(OH) 2vitamin D3 increased as pregnancy progressed. Serum levels of calcitonin (CT) in maternal serum increased late in pregnancy but were statistically not significant. Calcium concentrations in maternal urine during pregnancy showed a slight decrease.
It is suggested that calcium absorption in the maternal intestine might be increased by the action of increased serum 1α, 25-(OH) 2vitamin D3, and the maternal bone during pregnancy might be kept at the same density as in non-pregnant women because increased CT protects the maternal skeleton by resisting the bone-resorbing activities of 1α, 25-(OH) 2 vitamin D3.
The concentrations of ionized calcium and CT in umbilical cord blood were higher, but those of PTH and 1α, 25-(OH) 2vitamin D3 were significantly lower than those of the maternal blood at term.
It is considered that an active transport mechanism may be involved in the transplacental supply of calcium, and calcium transport from mother to fetus results in a decrease in the calcium concentrations of the maternal serum. Calcium transported into the fetus may be used as fetal body composition such as accumulation in the bone mainly by the action of serum CT.抄録全体を表示PDF形式でダウンロード (1092K) -
森本 勲夫, 和泉 元衛, 長瀧 重信, 岩崎 宏, 計屋 慧實1986 年 62 巻 7 号 p. 797-806
発行日: 1986/07/20
公開日: 2012/09/24
ジャーナル フリーBlood-free testosterone indices were measured among 28 normal men (age; 24-48 yrs.), 20 normal women (20-36 yrs.), 18 pregnant women (22-31 yrs.), 17 males with hypogonadism (23-56 yrs.), 17 males with chronic hepatitis (20-42 yrs.), 24 males with liver cirrhosis (29-68 yrs.), 34 males with hyperthyroidism (20-42 yrs.) and 7 hirsute women (18-31 yrs.), and these were compared with the plasma concentrations of free testosterone. The testosterone index was obtained by multiplying the plasma concentration of testosterone by the percent of sex hormone-binding globulin (SHBG), non-bound testosterone precipitated by dextran-coated charcoal. A significant increase of plasma testosterone was observed in patients with chronic hepatitis (p<0.001) and hyperthyroidism (p<0.001) as compared with normal men and was also observed in pregnant (p<0.01) and hirsute women (p<0.01) as compared with normal women. The close negative correlation between plasma levels of testosterone and the percent of SHBG non-bound testosterone (r=-0.87, n=79, p<0.001) was observed among normal men, male patients with chronic hepatitis and hyperthyroidism. The sex hormone binding capacity was increased from two to three fold in patients with chronic hepatitis and hyperthyroidism. The patients with compensated liver cirrhosis had increased plasma testosterone and a decreased percent of SHBG non-bound testosterone, and those with decompensated liver cirrhosis had decreased plasma testosterone and a normal percent of SHBG non-bound testosterone. The plasma concentration of free testosterone was normal in patients with chronic hepatitis and hyperthyroidism. It decreased in pregnancy (p<0.01) and increased in hirsute women (p<0.01). The blood free testosterone index was slightly high in one third of the patients with chronic hepatitis and hyperthyroidism as compared with that in normal men. However, a close correlation of the percent of SHBG non-bound testosterone and fractional free testosterone (%) measured by equilibrium dialysis (7=0.82, p<0.001) was obtained in all subjects (n= 170). These data suggest that the blood free testosterone index parallels the plasma concentration of free testosterone and is useful to evaluate the status of androgeneity.抄録全体を表示PDF形式でダウンロード (853K) -
Phorbol ester, 及びDiacylglycerolのラット膵腺房細胞細胞膜へのソマトスタチン結合に及ぼす効果的崎 尚, 坂本 長逸, 長尾 宗彦, 馬場 茂明1986 年 62 巻 7 号 p. 807-817
発行日: 1986/07/20
公開日: 2012/09/24
ジャーナル フリーTo clarify the precise mechanism by which unrelated peptides, cholecystokinin or carbamylcholine, modulate the somatostatin binding, the effect of a phorbol ester, 12-0-tetradecanoylphorbol-13-acetate (TPA) or a synthetic diacylglycerol analog, [125 I-Tyr1-oley1-2-acetylglycerol (OAG) onsomatostatin binding to pancreatic acinar cell membranes was examined.
Pretreatment of pancreatic acini for 120 min at 37°C with 100 ng/ml TPA maximally reduced subsequent labeled somatostatin binding to acinar membranes. The inhibitory effect of TPA on the somatostatin binding was dependent on the dose used, or the time and temperature of pretreatment. These effects of TPA were almost mimicked by the treatment of acini with OAG. Scatchard analysis of [125I-Tyr1 somatostatin binding demonstrated that the decrease in the labeled somatostatin binding induced by TPA or OAG pretreatment was due to the decrease in the maximum binding capacity without a significant change in the binding affinity.
A specifically labeled single band of the Mr = 90 K obtained with a photoaffinity crosslinking study indicates that the somatostatin binding sites are the same somatostatin receptor as previously described. Moreover, the intensity of the Mr = 90 K band was dramatically decreased when acini were treated with increasing concentrations of TPA, a finding consistent with TPA-induced decrease in binding capacity. Such an inhibitory effect of TPA was abolished when pretreatment of acini with TPA was performed in the presence of Ca 2+ chelating compounds such as EDTA and EGTA.
Interestingly, the combined treatment of TPA and Ca2+ionophore A23187 caused synergistic inhibition of the subsequent labeled somatostatin binding to acinar membranes, although Ca2+ionophore itself almost failed to affect the somatostatin binding.
These results suggest, therefore, that 1) TPA or OAG can modulate somatostatin binding to its receptors on rat pancreatic acinar cell membranes, presumably through activation of Ca2+-activated, phospholipid-dependent protein kinase (protein kinase C) and 2) the activated protein kinase C and intracellular Ca2+mobilization presumably act to modulate pancreatic acinar somatostatin receptors synergistically.抄録全体を表示PDF形式でダウンロード (1098K) -
-第一報-C端octapeptide CCK, carbachol前処理のsomatostatin結合抑制効果坂本 長逸, 的崎 尚, 長尾 宗彦, 馬場 茂明1986 年 62 巻 7 号 p. 818-826
発行日: 1986/07/20
公開日: 2012/09/24
ジャーナル フリーSomatostatin binding to its receptors on rat pancreatic acinar membranes was characterized with [125I-Tyr1 somatostatin. The COOH-terminal octapeptide of cholecystokinin (CCK8), when present at various concentrations in the reaction mixture for the binding study, reduced labeled somatostatin binding in a dose-dependent manner, whereas carbachol or Ca2+ ionophore did not affect the binding. By contrast, when pancreatic acini were first treated with carbachol and thereafter [125I-Tyr1 somatostatin binding to membranes prepared from these acini was examined, carbachol reduced subsequent somatostatin binding in a dose-dependent manner. Scatchard analysis of the labeled somatostatin binding revealed that carbachol pretreatment decreased the maximum binding capacity from 142±20 fmol/ mg of membrane protein to 63.5±3.5 fmol/mg of membrane protein without significantly affecting the binding affinity. To test for the possibility that CCK8 also may affect labeled somatostatin binding through an intracellular process, pancreatic acini were first treated with CCK8 and then the membrane bound CCK8 was washed out. Subsequent labeled somatostatin binding to membranes from these acini was also decreased. When 1 mM EDTA was present in the pretreatment medium, the inhibitory effect of carbachol or CCK8 was partially abolished, suggesting that an intracellular process to modulate somatostatin binding is dependent on Ca2+. On the other hand, pretreatment of acini with Ca2+ionophore almost failed to affect subsequent labeled somatostatin binding.
Results therefore suggest that 1) CCK8 can modulate labeled somatostatin binding to pancreatic acinar membranes not only acting through an intracellular process but also at membrane sites and 2) carbachol-or CCK8-activated intracellular process to modulate somatostatin binding is dependent on Ca2+, but Ca2+mobilization itself is not sufficient to affect subsequent somatostatin binding.抄録全体を表示PDF形式でダウンロード (793K)
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