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Gene regulation of atrial natriuretic peptide A, B, and C receptors in rat glomeruli. 大鼠肾小球心房利钠肽A、B和C受体的基因调控。
Pub Date : 1999-07-01 DOI: 10.1159/000020621
K Itoh, H Nonoguchi, N Shiraishi, K Tomita

Background and methods: Atrial natriuretic peptide (ANP) has three types of receptor. We investigated the gene regulation of three types of ANP receptors (ANPR-A, B, and C) in rat glomeruli using reverse transcription coupled with competitive polymerase chain reaction (PCR).

Results: Competitive PCR revealed that ANPR-C mRNA expression was most abundant (ANPR-C > A >> B) in glomeruli from control rats among mRNA expressions of three receptors, which were 20- to 15,000-fold higher than those in inner medullary collecting ducts. Two days' dehydration caused reversible decreases of ANPR-A, B, and C mRNAs by 50-80%. To determine the mechanisms of down-regulation of mRNA expression, isolated glomeruli were incubated in isotonic or hypertonic solution. Hyperosmolality induced by NaCl, mannitol or raffinose caused significant increases of ANPR-A, B, and C mRNA expression. Hypertonicity by urea showed smaller effects. ANP stimulated the expression of ANPR-A, B, and C mRNA in vitro.

Conclusion: These results indicate that dehydration caused reversible decreases of ANPR-A, B, and C mRNA expression in glomeruli, and these decreases were not caused by increased plasma osmolality but probably by lower circulating levels of ANP.

背景与方法:心房利钠肽(ANP)有三种受体。我们利用反转录和竞争性聚合酶链反应(PCR)技术研究了大鼠肾小球中三种ANP受体(ANPR-A、B和C)的基因调控。结果:竞争性PCR结果显示,三种受体mRNA表达量中,对照大鼠肾小球中ANPR-C mRNA表达量最高(ANPR-C > A > B),比髓内集管高20 ~ 1.5万倍。脱水2天导致ANPR-A、B和C mrna可逆降低50-80%。为了确定mRNA表达下调的机制,将离体肾小球置于等渗或高渗溶液中孵育。NaCl、甘露醇和棉子糖诱导的高渗可显著增加ANPR-A、B和C mRNA的表达。尿素的高渗作用较小。ANP刺激体外ANPR-A、B和C mRNA的表达。结论:脱水引起肾小球内ANPR-A、B和C mRNA表达的可逆性降低,这种降低可能与血浆渗透压升高无关,而可能与循环ANP水平降低有关。
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引用次数: 12
L-Histidinol attenuates Fanconi syndrome induced by ifosfamide in rats. 组氨酸二醇减轻异环磷酰胺所致大鼠范可尼综合征。
Pub Date : 1999-07-01 DOI: 10.1159/000020620
O A Badary

The effect of L-histidinol (LHL), a structural analogue of the essential amino acid L-histidine, on ifosfamide (IFO) induced nephrotoxicity was investigated in the rat. The aim of this study was to assess whether oral supplementation of LHL could attenuate Fanconi syndrome (FS) induced by IFO. Male Wistar albino rats received daily injections of IFO (50 mg/kg) for 5 days with or without oral supplementation of 0.5% LHL in the drinking water. LHL was supplemented for 3 days before IFO administration and daily thereafter. Control rats were injected with saline with or without oral LHL. The results demonstrated that IFO induces a FS characterized by wasting of glucose, electrolytes, and organic acids, along with elevated serum creatinine and urea levels and decreased creatinine clearance. IFO-induced FS was associated with significant renal nonprotein sulfhydryl depletion and lipid peroxide (malondialdehyde) accumulation. LHL strongly ameliorated the severity of renal dysfunction induced by IFO, with significant decreases in total and fractional excretions of Na(+), K(+), PO(4)(3-), and glucose. Also, LHL significantly decreased the elevated serum creatinine and urea levels and significantly increased the creatinine clearance. Moreover, the beneficial effects of LHL were associated with a significant improvement of IFO-induced nonprotein sufhydry depletion and lipid peroxide accumulation. These results demonstrate that oral supplementation of LHL can partially protect against IFO-induced FS in rats.

研究了必需氨基酸l -组氨酸的结构类似物l -组氨酸醇(LHL)对异环磷酰胺(IFO)引起的大鼠肾毒性的影响。本研究的目的是评估口服补充LHL是否可以减轻IFO诱导的范可尼综合征(FS)。雄性Wistar白化大鼠每天注射IFO (50 mg/kg),连续5天,同时或不在饮用水中口服添加0.5% LHL。在IFO给药前3天补充LHL,之后每天补充。对照组大鼠分别注射含或不含口服LHL的生理盐水。结果表明,IFO诱导FS的特征是葡萄糖、电解质和有机酸的消耗,同时血清肌酐和尿素水平升高,肌酐清除率降低。ifo诱导的FS与肾脏非蛋白巯基消耗和脂质过氧化(丙二醛)积累有关。LHL可显著改善IFO所致肾功能障碍的严重程度,显著降低Na(+)、K(+)、PO(4)(3-)和葡萄糖的总排泄量和部分排泄量。同时,LHL显著降低血清肌酐和尿素水平升高,显著增加肌酐清除率。此外,LHL的有益作用与ifo诱导的非蛋白脱水和脂质过氧化积累的显著改善有关。这些结果表明,口服补充LHL对ifo诱导的大鼠FS有一定的保护作用。
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引用次数: 19
Regulation of dopamine-induced natriuresisby the dopamine-metabolizing enzyme catechol-O-methyltransferase. 多巴胺代谢酶儿茶酚- o -甲基转移酶对多巴胺诱导的耐钠性的调节。
Pub Date : 1999-07-01 DOI: 10.1159/000020619
C Odlind, V Göransson, I Reenilä, P Hansell

Dopamine (DA) is an intrarenal natriuretic hormone involved in sodium homeostasis. A study was performed to elucidate two possible regulatory pathways of DA-induced natriuresis, i.e., metabolism and precursor delivery. This was done by use of an intraperitoneal injection of a catechol-O-methyltransferase (COMT) inhibitor, entacapone, or intravenous infusion of the DA precursor, L-dopa. Entacapone (30 mg/kg i.p.) induced a more than fivefold increase in renal sodium excretion which occurred without changes in renal haemodynamics. The natriuretic response was highly dependent on DA D(1)-like receptor activation, since the selective D(1)-like receptor antagonist SCH23390 attenuated the natriuretic response by 61%, while the selective D(2)-like receptor antagonist sulpiride was ineffective. The urinary excretion of DA did not increase. Infusion of L-dopa (60 microg/h/kg) only induced a twofold increase in sodium excretion, but the urinary excretion of DA increased more than 17-fold. The L-dopa-induced natriuretic response occurred without increments in glomerular filtration rate and could be blocked with the D(1)-like receptor antagonist SCH23390. It is concluded that the DA-metabolizing enzyme COMT is involved in the regulation of the natriuretic effect of intrarenal DA. It may be speculated that intrarenal DA activity is not primarily determined on the basis of delivered precursor, but on that of the level of DA metabolism.

多巴胺(DA)是一种参与钠稳态的肾内利钠激素。我们进行了一项研究,以阐明两种可能的调控途径,即代谢和前体递送。这是通过使用腹腔注射儿茶酚o -甲基转移酶(COMT)抑制剂恩他卡酮或静脉输注DA前体左旋多巴来完成的。恩他卡朋(30mg /kg i.p)诱导肾钠排泄量增加5倍以上,而肾血流动力学没有改变。利钠反应高度依赖于DA D(1)样受体的激活,因为选择性D(1)样受体拮抗剂SCH23390可将利钠反应减弱61%,而选择性D(2)样受体拮抗剂舒必利无效。尿中DA的排泄量没有增加。输注左旋多巴(60 μ g/h/kg)仅诱导钠排泄量增加2倍,但尿中DA排泄量增加17倍以上。左旋多巴诱导的利钠反应没有增加肾小球滤过率,可以用D(1)样受体拮抗剂SCH23390阻断。由此可见,DA代谢酶COMT参与了肾内DA的利钠作用的调控。由此可以推测,决定肾内DA活性的主要不是递送的前体,而是DA代谢水平。
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引用次数: 18
Nuclear protein transport pathways. 核蛋白转运途径。
Pub Date : 1999-07-01 DOI: 10.1159/000020616
M Köhler, H Haller, E Hartmann

Nuclear proteins like transcription factors and ribosomal proteins are synthesized in the cytoplasm and have to be transported into the nucleus to fulfill their functions. The transport of proteins >20-60 kD through the nuclear pore complex (NPC) into the nucleus is an active, energy-requiring process. Transport substrates are recognized by their transport proteins via certain signals. The best-characterized protein import pathway is the 'classical' nuclear localization signal-dependent pathway with importin alpha and beta carrying the substrate to the NPC. The transport of the importin-substrate complex into the nucleus is regulated by the small GTPase Ran/TC4. During the last years more than ten proteins have been discovered which have already been proven or are very likely to be nuclear transport factors of distinct import pathways: members of the importin alpha protein family are very similar and transport in complex with importin beta nuclear localization signal-bearing proteins into the nucleus. Members of the Ran-binding protein family show some weak similarity to importin beta. Sharing a common domain at the amino terminus, they are able to bind RanGTP, a prerequisite for their function as nuclear import or export factors for distinct proteins or RNAs. However, Ran/TC4 seems to play a key regulatory role in all nuclear transport pathways described so far, although the molecular mechanism of the translocation step through the NPC is still unclear.

像转录因子和核糖体蛋白这样的核蛋白是在细胞质中合成的,必须被运送到细胞核中才能完成它们的功能。>20- 60kd的蛋白质通过核孔复合物(NPC)进入细胞核是一个主动的、需要能量的过程。转运底物被转运蛋白通过一定的信号识别。最具特征的蛋白质输入途径是“经典的”核定位信号依赖途径,其输入蛋白α和β将底物携带到NPC。进口蛋白-底物复合物进入细胞核的运输是由小GTPase Ran/TC4调控的。在过去的几年里,已经发现了十多种蛋白质,这些蛋白质已经被证明或很可能是具有不同进口途径的核转运因子:进口蛋白α家族的成员非常相似,并且与进口蛋白β核定位信号携带蛋白复杂地转运到细胞核中。ran结合蛋白家族的成员与输入β蛋白有微弱的相似性。它们在氨基端有一个共同的结构域,能够结合RanGTP,这是它们作为不同蛋白质或rna的核输入或输出因子功能的先决条件。然而,Ran/TC4似乎在迄今所描述的所有核转运途径中起着关键的调节作用,尽管通过NPC的转运步骤的分子机制尚不清楚。
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引用次数: 32
Transdifferentiation of distal but not proximal tubular epithelial cells from human kidney in culture. 培养人肾远端而非近端小管上皮细胞的转分化。
Pub Date : 1999-07-01 DOI: 10.1159/000020618
P C Baer, U W Tunn, G Nunez, J E Scherberich, H Geiger

Human renal proximal and distal (thick ascending limb and early distal convoluted tubule) epithelial cells have been isolated according to their specific antigen expression. The cells were well characterized by flow cytometry, enzyme cytochemistry and electron microscopy and cultured for up to 3 months. Cultured tubular cells coexpressed cytokeratin and vimentin as intermediate filament proteins. While primary isolated cells, proximal as well as distal, revealed the phenotypic characteristics of their nephron origin, cultured distal cells showed the tendency to dedifferentiate/transdifferentiate. Distal cells lost their characteristic expression of Tamm-Horsfall glycoprotein and started de novo expression of the proximal marker proteins aminopeptidase M, gamma-glutamyl transferase and dipeptidyl peptidase IV. The expression of these antigens by distal cells could be shown by flow-cytometric analysis and fluorescence microscopy. Enzyme activity assays revealed the activity of aminopeptidase M, gamma-glutamyl transferase and dipeptidyl peptidase IV, but not of the proximal marker enzyme alkaline phosphatase. This antigenic shift could not be prevented in different culture media, and the original phenotype could not be restored. Cultured cells displayed characteristic hormonal stimulation patterns indicative of their proximal and distal origins, as shown by activation of adenylate cyclase by different peptide hormones. These results indicate that distal tubular cells possibly transdifferentiate to a more proximal phenotype in view of loss of the distal marker enzyme Tamm-Horsfall protein and de novo expression of proximal marker enzymes like dipeptidyl peptidase IV and aminopeptidase M.

人肾近端和远端(厚升肢和早期远端曲小管)上皮细胞已根据其特异性抗原表达分离。流式细胞术、酶细胞化学和电镜对细胞进行了很好的表征,并培养了3个月。培养的小管细胞共表达细胞角蛋白和波形蛋白作为中间丝蛋白。虽然原代离体细胞(近端和远端)显示出其肾元来源的表型特征,但培养的远端细胞显示出去分化/转分化的倾向。远端细胞失去了Tamm-Horsfall糖蛋白的特征表达,并开始重新表达近端标记蛋白氨基肽酶M、γ -谷氨酰转移酶和二肽基肽酶IV。这些抗原在远端细胞中的表达可以通过流式细胞分析和荧光显微镜显示。酶活性测定显示氨肽酶M、γ -谷氨酰转移酶和二肽基肽酶IV有活性,但近端标记酶碱性磷酸酶无活性。这种抗原转移在不同的培养基中都不能被阻止,并且不能恢复原来的表型。通过不同的肽激素对腺苷酸环化酶的激活,培养的细胞显示出其近端和远端来源的特征性激素刺激模式。这些结果表明,考虑到远端标记酶Tamm-Horsfall蛋白的缺失和近端标记酶如二肽基肽酶IV和氨基肽酶M的重新表达,远端小管细胞可能会转分化为更近端的表型。
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引用次数: 34
Transfer of genetically engineered cells to the glomerulus. 将基因工程细胞转移到肾小球。
Pub Date : 1999-05-01 DOI: 10.1159/000020611
M Kitamura

In the rat, cultured cells injected into the renal circulation are entrapped in the glomerulus. This peculiar property allows to create chimeric glomeruli in which genetically engineered cells are populated. Using glomerular cells engineered in vitro, it is feasible to generate glomeruli that produce recombinant gene products. This approach would be useful for identification of local function of a certain gene product in the glomerulus and for therapeutic intervention in glomerular disease. Transfer of activated leukocytes to the glomerulus is useful to elucidate pathologic actions of infiltrating cells on the glomerular structure and function. Use of leukocytes in which certain gene function is selectively reinforced or deleted should enable to disclose exact roles of leukocyte-associated genes in glomerular pathophysiology. Transfer of engineered leukocytes also allows to investigate how resident cells modulate the activity of infiltrating cells in normal and pathologic circumstances. This article summarizes current experience with adoptive transfer of engineered cells to the glomerulus and addresses its potential application to kidney research.

在大鼠中,注入肾循环的培养细胞被困在肾小球中。这种特殊的特性允许产生嵌合肾小球,其中填充了基因工程细胞。利用体外工程改造的肾小球细胞,可以产生产生重组基因产物的肾小球。这种方法将有助于确定肾小球中某种基因产物的局部功能,并有助于肾小球疾病的治疗干预。活化白细胞向肾小球的转移有助于阐明浸润细胞对肾小球结构和功能的病理作用。使用某些基因功能被选择性增强或删除的白细胞,应该能够揭示白细胞相关基因在肾小球病理生理中的确切作用。工程白细胞的转移也允许研究在正常和病理情况下驻留细胞如何调节浸润细胞的活性。本文总结了目前工程细胞过继转移到肾小球的经验,并讨论了其在肾脏研究中的潜在应用。
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引用次数: 2
Effect of human natural xenoantibody depletion and complement inactivation on early pig kidney function. 人天然异种抗体去除和补体失活对早期猪肾功能的影响。
Pub Date : 1999-05-01 DOI: 10.1159/000020605
J M Cruzado, J Torras, M Riera, E Condom, N Lloberas, I Herrero, J Martorell, J M Grinyó

Preformed xenoreactive natural antibodies (XNA) and complement mediate hyperacute xenograft rejection (HXR) in pig-to-human discordant xenotransplantation. In a pig kidney-human blood xenoperfusion model, we investigated whether XNA depletion and/or human complement inactivation preserved early pig kidney function. Pig kidneys were perfused for 180 min with pig blood (AUTO group, n = 8), human blood (HETER group, n = 6), complement-inactivated human blood (COMi group, n = 5), XNA-depleted human blood (ABd group, n = 5) or complement-inactivated and XNA-depleted human blood (ABd&COMi group, n = 5). HETER kidneys were rejected after 15-30 min and showed vascular microthrombi and interstitial hemorrhages. XNA depletion and/or complement inactivation prevented HXR. The glomerular filtration rate in ABd, COMi and ABd&COMi groups was significantly lower than in the AUTO group. Also, beyond 60 min, the COMi group showed a significantly lower glomerular filtration rate than that observed in ABd and ABd&COMi groups. Kidneys from ABd, COMi and ABd&COMi groups displayed endothelial cell edema, as well as higher soluble P-selectin levels and a higher renal myeloperoxidase content than the AUTO group kidneys. COMi and ABd&COMi groups had a significantly lower renal myeloperoxidase level than the HETER group. Also, in contrast to HETER and ABd groups, these complement-inactivated groups failed to show a positive correlation between P-selectin and renal myeloperoxidase. We also investigated platelet-activating factor (PAF) as possible mediator for these functional and pathologic changes. We found that blood PAF levels were similar in HETER, ABd, COMi and ABd&COMi groups and significantly higher than in the AUTO group. Also, when PAF was added to porcine endothelial cell monolayers, morphological changes due to cytoskeleton contraction were observed, and these changes were prevented by preincubation with a PAF receptor antagonist. In conclusion, although depletion of XNA and/or complement inactivation prevent HXR, the pig kidney function is not preserved at the level of the autologous combination. The PAF overproduction observed in the xenogenic combination, which is independent of the presence of XNA and complement, may be, at least in part, responsible for early endothelial cell morphological changes still present when HXR is prevented.

预先形成的异种反应性天然抗体(XNA)和补体介导猪到人不协调异种移植的超急性异种移植排斥反应(HXR)。在猪肾-人血异种灌注模型中,我们研究了XNA缺失和/或人补体失活是否能保留早期猪的肾功能。用猪血(AUTO组,n = 8)、人血(HETER组,n = 6)、补体失活人血(COMi组,n = 5)、去xna人血(ABd组,n = 5)或去xna补体失活人血(ABd&COMi组,n = 5)灌注猪肾180 min, HETER肾在15-30 min后出现排斥反应,出现血管微血栓和间质性出血。XNA耗竭和/或补体失活可预防HXR。ABd组、COMi组及ABd&COMi组肾小球滤过率均显著低于AUTO组。此外,超过60分钟,COMi组的肾小球滤过率明显低于ABd和ABd&COMi组。与AUTO组相比,ABd组、COMi组和ABd&COMi组肾脏内皮细胞水肿,可溶性p -选择素水平较高,肾髓过氧化物酶含量较高。COMi组和ABd&COMi组肾髓过氧化物酶水平明显低于HETER组。此外,与HETER和ABd组相比,这些补体失活组未能显示p选择素和肾髓过氧化物酶之间的正相关。我们还研究了血小板活化因子(PAF)作为这些功能和病理变化的可能中介。我们发现血PAF水平在HETER、ABd、COMi和ABd&COMi组相似,且显著高于AUTO组。此外,当将PAF添加到猪内皮细胞单层时,观察到细胞骨架收缩引起的形态学变化,这些变化可以通过PAF受体拮抗剂预孵育来防止。综上所述,尽管XNA的消耗和/或补体失活可以预防HXR,但猪的肾功能不能维持在自体联合的水平。在异种组合中观察到PAF的过量产生,它独立于XNA和补体的存在,可能至少部分地负责早期内皮细胞形态变化,当HXR被阻止时仍然存在。
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引用次数: 2
Cell cycle regulatory proteins in glomerular disease. 肾小球疾病中的细胞周期调节蛋白。
Pub Date : 1999-05-01 DOI: 10.1159/000020603
S J Shankland, M Al'Douahji

The growth response of resident glomerular cells is determined by the underlying disease. Thus glomerular cells can proliferate, fail to proliferate, hypertrophy or apoptose. Cell growth is controlled by cell cycle regulatory proteins, and cell proliferation requires that cyclin-dependent kinases (CDK) be activated by partner cyclins. Inhibiting CDK2 reduces mesangial cell proliferation. Mesangial cell proliferation also requires that levels of specific cyclin kinase inhibitors (CKI) decrease. In contrast, the visceral glomerular epithelial cells' inability to proliferate may be due to increased levels of CKI. Moreover it is becoming increasingly clear that mesangial cell hypertrophy in diabetes requires increased CKI expression. Finally, apoptosis, which is often linked to proliferation, may also be due to the increased activity of CDK2. Thus, identifying specific cell cycle regulatory proteins following injury may provide future targets for therapy in glomerular disease.

常驻肾小球细胞的生长反应是由潜在疾病决定的。因此肾小球细胞可以增殖、不增殖、肥大或凋亡。细胞生长受细胞周期调节蛋白控制,细胞增殖需要周期蛋白依赖性激酶(CDK)被伴侣周期蛋白激活。抑制CDK2可减少系膜细胞增殖。系膜细胞增殖也需要特异性细胞周期蛋白激酶抑制剂(CKI)水平的降低。相反,内脏肾小球上皮细胞不能增殖可能是由于CKI水平升高。此外,越来越清楚的是,糖尿病的系膜细胞肥大需要CKI表达增加。最后,通常与增殖有关的细胞凋亡也可能是由于CDK2活性的增加。因此,鉴定损伤后特定的细胞周期调节蛋白可能为肾小球疾病的治疗提供未来的靶点。
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引用次数: 30
Inhibition of erythrocyte aminolevulinate dehydratase by a 56.2-kD peptide from uremic plasma. 尿毒症血浆中56.2 kd肽对红细胞氨基乙酰酸脱水酶的抑制作用。
Pub Date : 1999-05-01 DOI: 10.1159/000020607
M Guolo, C Machalinski, M Biscoglio, A M Stella, C Franco, L Pataro, R E de Salamanca, A Batlle

Among the abnormalities in erythrocyte porphyrin metabolism already described in patients with chronic renal failure on hemodialysis, a decrease in blood aminolevulinate dehydratase activity has been reported, suggesting the presence in uremic plasma of an inhibitor of the enzyme. The aim of this work has been to isolate and characterize such an inhibitor. Blood samples from 105 patients with chronic uremia were collected; plasma was applied to Sephadex G-100 columns and the fraction with the highest inhibiting capacity was identified and purified by subsequent SDS-polyacrylamide gel electrophoresis, followed by electroelution and electroblotting. It was demonstrated that the factor present in plasma of uremic patients inhibited blood aminolevulinate dehydratase in a concentration-dependent manner; its inhibitory properties were abolished after heat, trypsin and TCA treatment indicating its peptidic nature. The purified inhibitor has an apparent molecular mass of 56.2 kD, it inhibits blood aminolevulinate dehydratase in a competitive way and the Ki value is 12x10(-6) M. The amino acid composition of the inhibitor has been determined and it has been found that its N-terminal amino acid is blocked. The isolated peptide may play a role in heme biosynthesis disturbances and in the pathogenesis of uremic anemia.

在血液透析慢性肾衰竭患者的红细胞卟啉代谢异常中,有报道称血液氨基乙酰酸脱水酶活性降低,提示尿毒症血浆中存在该酶的抑制剂。这项工作的目的是分离和表征这种抑制剂。收集105例慢性尿毒症患者的血液样本;将血浆应用于Sephadex G-100色谱柱,通过sds -聚丙烯酰胺凝胶电泳鉴定和纯化抑制能力最高的部分,然后进行电洗脱和电泳印迹。结果表明,该因子存在于尿毒症患者血浆中,呈浓度依赖性地抑制血氨乙酰酸脱水酶;经高温、胰蛋白酶和TCA处理后,其抑制作用被消除,表明其具有肽性。纯化后的抑制剂表观分子质量为56.2 kD,以竞争方式抑制血氨酰酸脱水酶,Ki值为12 × 10(-6) m。测定了该抑制剂的氨基酸组成,发现其n端氨基酸被阻断。分离的肽可能在血红素生物合成紊乱和尿毒症的发病机制中发挥作用。
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引用次数: 9
Regulation of the ROMK potassium channel in the kidney. 肾中ROMK钾通道的调节。
Pub Date : 1999-05-01 DOI: 10.1159/000020602
H Wald

ROMK is a gene encoding inwardly rectifying adenosine triphosphate regulated K+ channels. Alternative splicing of ROMK exons yields several different transcripts, ROMK 1-3, that are differentially expressed along the nephron. Cloned ROMK channels expressed in Xenopus oocytes exhibit properties similar to those of the native low-conductance K+ secretory channels in cortical collecting duct and medullary thick ascending limb, as manifested by use of the patch-clamp technique. These similarities between the cloned and native channels suggest that ROMK represents the low-conductance secretory K+ channels in the kidney. We studied the role of dietary K+ and aldosterone in the regulation of ROMK mRNA expression in the rat kidney. K+ deficiency downregulated ROMK mRNA in cortex and medulla. Adrenalectomy markedly downregulated cortical ROMK, while it increased it in the medulla. In adrenalectomized rats K+ deficiency decreased ROMK mRNA in cortex and medulla similarly to intact rats. Na-K-ATPase subunits alpha1 and beta1 were regulated in parallel to the regulation of ROMK. In the medulla ROMK mRNA correlated highly with serum K+ and with the alpha1 and beta1 subunits of Na-K-ATPase. These results show that cortical ROMK expression is regulated by aldosterone and K+, while the medullary ROMK mRNA is regulated by serum K+, irrespective of aldosterone.

ROMK是一种编码向内校正三磷酸腺苷调节的K+通道的基因。ROMK外显子的选择性剪接产生几种不同的转录本,ROMK 1-3,它们沿着肾元不同地表达。膜片钳技术显示,爪蟾卵母细胞中表达的克隆ROMK通道具有与皮质集管和髓质厚升肢中天然低电导K+分泌通道相似的特性。克隆通道和天然通道之间的这些相似性表明ROMK代表肾脏中低电导分泌K+通道。我们研究了膳食K+和醛固酮在大鼠肾脏中对ROMK mRNA表达的调节作用。K+缺乏下调皮质和髓质的ROMK mRNA。肾上腺切除术显著下调皮质ROMK,而增加髓质的ROMK。在肾上腺切除的大鼠中,K+缺乏降低了皮质和髓质的ROMK mRNA,与完整大鼠相似。na - k - atp酶亚基α 1和β 1的调控与ROMK的调控平行。在髓质中,ROMK mRNA与血清K+以及na -K- atp酶的α 1和β 1亚基高度相关。这些结果表明,皮质ROMK mRNA的表达受醛固酮和K+的调节,而髓质ROMK mRNA受血清K+的调节,与醛固酮无关。
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引用次数: 6
期刊
Experimental nephrology
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