A Role of Subcellular Factors to Control Channels in Kidney Tubules.
亚细胞因子控制肾小管通道的作用。
基本信息
- 批准号:01570040
- 负责人:
- 金额:$ 1.34万
- 依托单位:
- 依托单位国家:日本
- 项目类别:Grant-in-Aid for General Scientific Research (C)
- 财政年份:1989
- 资助国家:日本
- 起止时间:1989 至 1990
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
Using the patch-clamp technique, we investigated a mechanism of activation of single-channel currents during cell volume regulation in cultured rabbit kidney proximal tubule cells. Hypotonically induced cell-swelling increased Ca-dependent K currents, and then, Cl currents. Because cell membrane potential initially hyperpolarized, and then returned to the original level with KCl in the pipette (current-clamp mode). Omitting extracellular Ca from and adding 0.1 mM EGTA to the bath solution significantly slowed a time course of cell volume regulation. At Vp=0 mV the whole-cell K currents induced by hypotonicity decreased by 90% when a pipette-filling solution contained zero Ca and 5 mM EGTA. Addition of 5 mM Ba to the bath almost completely inhibited K currents due to cell-swelling. Activation of Cl currents due to hypotonicity was partially inhibited by either 20 uM SITS in the bath or zero Ca plus 5 mMEGTA in the pipette(whole-cell clamp condition).In conclusion, hypotonicallyinduced cell swelling stimulates Ca-activated K channels, which may play an important role in cell volume regulation. A secondary activation of Cl currents may also be essential for the regulatory volume decrease mechanism.
应用膜片钳技术,研究了体外培养的兔肾近端小管细胞容量调节过程中单通道电流激活的机制。低渗引起的细胞肿胀增加钙依赖性钾电流,然后,氯电流。因为细胞膜电位最初超极化,然后在移液器中用KCl恢复到原始水平(电流钳模式)。省略细胞外钙和添加0.1 mM EGTA浴溶液显着减缓了细胞体积调节的时间过程。在Vp=0 mV时,低渗诱导的全细胞K电流下降了90%,当移液管填充溶液中含有零Ca和5 mM EGTA时。加入5 mM Ba的浴几乎完全抑制K电流由于细胞肿胀。低渗引起的Cl-电流激活被20 μ M SITS或5 mMEGTA加0 Ca(全细胞钳夹)部分抑制。总之,低渗引起的细胞肿胀刺激Ca激活的K通道,这可能在细胞容积调节中起重要作用。二次激活的Cl电流也可能是必不可少的监管量减少机制。
项目成果
期刊论文数量(16)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Giebisch,G.: "Apical potassium channels in Amphiuma diluting segment:Effect of barium" J.Physiology(Lond.). 420. 313-323 (1990)
Giebisch,G.:“Amphiuma 稀释段中的顶端钾通道:钡的作用”J.Physiology(伦敦)。
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河原克雅: "腎におけるイオンチャネル" 腎と透析. 26. 553-555 (1989)
Katsumasa Kawahara:“肾脏中的离子通道”《肾脏与透析》26. 553-555 (1989)。
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- 影响因子:0
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KAWAHARA,K.: "A stretchーactivated K^+ channel in the basolcteral membrane of xenopus Kidney proximal tubule cells." Ptlugers Ard Europedn J.of Physiol.415. 624-629 (1990)
KAWAHARA, K.:“爪蟾肾近端小管细胞基底膜中的拉伸激活 K^+ 通道。”Ptlugers Ard Europedn J.of Physiol.415 (1990)。
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Kawahara,K.: "“Flickery block"of Ca-activated K channels by intracellular Na in the luminal membrane of Amphiuma diluting segment" Pfluegers Arch.(1990)
Kawahara, K.:“Amphiuma 稀释段管腔膜中细胞内 Na 对 Ca 激活 K 通道的“闪烁阻断””Pfluegers Arch.(1990)
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- 影响因子:0
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KAWAHARA, K.: "A Stretch-Activated K Channel in the Basolateral Membrane of Xenopus Kidney Proximal Tubule Cells." Pfluegers Arch. 415. 624-629 (1990)
KAWAHARA, K.:“非洲爪蟾肾近端小管细胞基底外侧膜中的拉伸激活 K 通道。”
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KAWAHARA Katsumasa其他文献
KAWAHARA Katsumasa的其他文献
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{{ truncateString('KAWAHARA Katsumasa', 18)}}的其他基金
A role of kidney K channel for acid-base regulation
肾钾通道对酸碱调节的作用
- 批准号:
23591224 - 财政年份:2011
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
REGULATION OF BODY WATER AND ELECTROLYTES CONCENTRATIONS BY RENAL NA/K/2CL TRANSPORTER (NKCC2)
肾脏 NA/K/2CL 转运蛋白 (NKCC2) 对体内水份和电解质浓度的调节
- 批准号:
11670050 - 财政年份:1999
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
EXPRESSION OF Na^+-DEPENDENT GLUCOSE TRANSPORTERS (SGLT1, SGLT2) IN RAT KIDNEY PROXIMAL TUBULES.
大鼠肾近端小管中Na^-依赖性葡萄糖转运蛋白(SGLT1、SGLT2)的表达。
- 批准号:
09670054 - 财政年份:1997
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
Electrophysiological and optical methods for ATP-receptor-operated calcium channels in kidney tubule cells.
肾小管细胞中 ATP 受体操纵的钙通道的电生理学和光学方法。
- 批准号:
05670038 - 财政年份:1993
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
Subcellular Regulation of Calcium Channel Currents in Renal Tubules.
肾小管钙通道电流的亚细胞调节。
- 批准号:
03670036 - 财政年份:1991
- 资助金额:
$ 1.34万 - 项目类别:
Grant-in-Aid for General Scientific Research (C)
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