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缓激肽、ATP和肾上腺素对犬肾Madin-Darby细胞细胞膜电阻的影响。

Effect of bradykinin, ATP and adrenaline on cell membrane resistances of Madin-Darby canine kidney cells.

作者信息

Ritter M, Lang F

机构信息

Institute for Physiology, University of Innsbruck, Austria.

出版信息

J Physiol. 1991 Nov;443:45-54. doi: 10.1113/jphysiol.1991.sp018821.

DOI:10.1113/jphysiol.1991.sp018821
PMID:1822532
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1179829/
Abstract
  1. Previous studies have shown that bradykinin, ATP and adrenaline hyperpolarize the cell membrane of Madin-Darby canine kidney (MDCK) cells by activation of calcium-sensitive K+ channels. The present study has been performed to determine the effect of these hormones on the resistance of the cell membrane and the cellular coupling. To this end, cellular cable analysis has been performed. 2. As a result, all three hormones lead to the expected, marked decrease of cell membrane resistance. 3. However, the bradykinin-induced reduction of cell membrane resistance was sustained, contrasting with only transient hyperpolarization induced by bradykinin and only transient activation of the K+ channels. Thus, the cable analysis reveals the sustained activation of an additional conductance. 4. ATP, but not the other two hormones, leads to a delayed increase of the intercellular coupling resistances. 5. Prolonged exposure of the cells to adrenaline leads to oscillations of the cell membrane potential, apparently by oscillatory activation of the K+ channels.
摘要
  1. 先前的研究表明,缓激肽、三磷酸腺苷(ATP)和肾上腺素通过激活钙敏感性钾离子通道,使犬肾传代细胞(MDCK)的细胞膜超极化。本研究旨在确定这些激素对细胞膜电阻和细胞耦联的影响。为此,进行了细胞电缆分析。2. 结果,所有这三种激素均导致细胞膜电阻出现预期的显著降低。3. 然而,缓激肽引起的细胞膜电阻降低是持续性的,这与缓激肽仅引起短暂的超极化以及仅短暂激活钾离子通道形成对比。因此,电缆分析揭示了另一种电导的持续激活。4. ATP会导致细胞间耦联电阻延迟增加,而其他两种激素则不会。5. 细胞长时间暴露于肾上腺素会导致细胞膜电位振荡,这显然是由钾离子通道的振荡激活引起的。

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引用本文的文献

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2
Cell shrinkage stimulates bradykinin-induced cell membrane potential oscillations in NIH 3T3 fibroblasts expressing the ras-oncogene.细胞皱缩刺激表达ras癌基因的NIH 3T3成纤维细胞中缓激肽诱导的细胞膜电位振荡。
Pflugers Arch. 1993 May;423(3-4):221-4. doi: 10.1007/BF00374398.

本文引用的文献

1
Kinins stimulate net chloride secretion by the rat colon.激肽刺激大鼠结肠的净氯化物分泌。
Br J Pharmacol. 1982 Apr;75(4):587-98. doi: 10.1111/j.1476-5381.1982.tb09178.x.
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Kinin effects on chloride secretion do not require eicosanoid synthesis.激肽对氯化物分泌的影响并不需要类花生酸的合成。
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Mediators of the secretory response to kinins.激肽分泌反应的介质。
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Bradykinin receptor-mediated chloride secretion in intestinal function.缓激肽受体介导的氯离子分泌在肠道功能中的作用
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6
Bradykinin-evoked modulation of cytosolic Ca2+ concentrations in cultured renal epithelial (MDCK) cells.缓激肽对培养的肾上皮(MDCK)细胞胞质Ca2+浓度的诱发调节作用。
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Kinin effects on electrogenic ion transport in primary cultures of pig renal papillary collecting tubule cells.激肽对猪肾乳头集合管细胞原代培养物中电生性离子转运的影响。
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Apparent chloride conductance of subconfluent Madin Darby canine kidney cells.亚汇合状态的麦迪逊-达比犬肾细胞的表观氯离子电导率。
Pflugers Arch. 1986 Aug;407(2):158-62. doi: 10.1007/BF00580668.
9
Effects of epinephrine on electrical properties of Madin-Darby canine kidney cells.肾上腺素对麦迪逊-达比犬肾细胞电特性的影响。
Pflugers Arch. 1986 Apr;406(4):367-71. doi: 10.1007/BF00590938.
10
Effects of bradykinin on electrical properties of Madin-Darby canine kidney epithelioid cells.缓激肽对犬肾Madin-Darby上皮样细胞电特性的影响。
Pflugers Arch. 1987 Apr;408(4):408-13. doi: 10.1007/BF00581137.