Hypotonic stress-induced release of KHCO3 in fused renal epitheloid (MDCK) cells.
Hypotonic stress-induced release of KHCO3 in fused renal epitheloid (MDCK) cells.
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低渗应激诱导融合肾上皮样 (MDCK) 细胞释放 KHCO3。
DOI：
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发表时间：
1991
影响因子：
19.6
通讯作者：
H. Oberleithner
中科院分区：
文献类型：
--
作者：
U. Kersting;L. Wojnowski;W. Steigner;H. Oberleithner
在融合的Madin-Darby犬肾（MDCK）细胞中研究了由林格溶液的渗透压降低三分之一诱导的细胞体积调节机制。用微电极技术测定了细胞内HCO 3-、K+和Cl-浓度[ion]i与细胞膜电位（PD）、细胞膜电导（Gm）和单个离子电导（Gmion）的关系。融合的细胞调节其细胞体积约50%。Gm从等渗林格溶液中的0.43 +/-0.03mS/cm2增加到细胞溶胀的稳态阶段中的4.3 +/-0.3mS/cm2。在等渗林格溶液中，GmCl为0.31 +/- 0.03 mS/cm 2，因此是主要的单个离子电导。在细胞肿胀的初始阶段，GmK瞬时增加64倍至0.32 +/- 0.03 mS/cm 2，因此PD超极化。在峰值超极化时，GmCl短暂降低15%。在细胞肿胀的稳态阶段，细胞肿胀使GmCl增加11倍，GmHCO 3增加28倍，达到0.95 +/- 0.1 mS/cm 2。在这个阶段，GmCl和GmHCO 3占主导地位，而GmK相比，等渗条件下，只有轻微增加。胞浆酸化可抑制PD的超极化。在峰值酸化[HCO 3-]i下降了6.4 mmol/kg H2O。在细胞肿胀的初始阶段，Cl-挤出是不可检测的。在等渗林格氏溶液中，[K+]i为125 +/- 5 mmol/kg H2O。在细胞膨胀的初始阶段，23 +/- 5 mmol/kg H2O K+被挤出，表明在细胞膨胀的这一阶段，还未知的阴离子参与细胞体积调节。在细胞溶胀的稳态阶段，[pH]i通过补充[HCO 3-]i而被归一化，而Cl-被挤出。我们的结论是，融合的肾上皮样细胞急性释放KHCO 3响应低渗，但随后恢复pH稳态阶段的细胞肿胀。
Mechanisms of cell volume regulation induced by the reduction of the osmolality of the Ringer solution by one-third were studied in fused Madin-Darby canine kidney (MDCK) cells. Intracellular HCO3-, K+ and Cl- concentrations [ion]i in parallel with cell membrane potential (PD), cell membrane conductance (Gm) and conductances of individual ions (Gmion) were evaluated with microelectrode techniques. Fused cells regulate their cell volume by about 50%. Gm increased from 0.43 +/- 0.03 mS/cm2 in isotonic Ringer solution to 4.3 +/-0.3 mS/cm2 in the steady state phase of cell swelling. GmCl was 0.31 +/- 0.03 mS/cm2 in isotonic Ringer solution and thus was the dominant individual ion conductance. In the initial phase of cell swelling GmK increased transiently 64-fold to 0.32 +/- 0.03 mS/cm2, and consequently PD hyperpolarized. At peak hyperpolarization GmCl transiently decreased by 15%. Cell swelling increased GmCl 11-fold and GmHCO3 28-fold to 0.95 +/- 0.1 mS/cm2 in the steady state phase of cell swelling. In this phase GmCl and GmHCO3 were dominating, whereas GmK was only slightly increased compared to isotonic conditions. The hyperpolarization of PD was paralleled by cytoplasmic acidification. At peak acidification [HCO3-]i decreased by 6.4 mmol/kg H2O. Cl- extrusion was not detectable in the initial phase of cell swelling. In isotonic Ringer solution [K+]i was 125 +/- 5 mmol/kg H2O. During the initial phase of cell swelling 23 +/- 5 mmol/kg H2O K+ was extruded, indicating that yet unknown anions participated in cell volume regulation in this phase of cell swelling. In the steady state phase of cell swelling [pH]i was normalized by replenishing [HCO3-]i, whereas Cl- was extruded. We conclude that fused renal epitheloid cells acutely release KHCO3 in response to hypotonicity, but then regain pH homeostasis in the steady state phase of cell swelling.
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DOI：
10.1073/pnas.81.13.4237
发表时间：
1984
影响因子：
11.1
作者：
Hunter,M;Lopes,AG;Boulpaep,EL;Giebisch,GH
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DOI：
10.1152/ajpcell.1986.251.3.c347
发表时间：
1986
期刊：
The American journal of physiology
影响因子：
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作者：
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Jennings,ML
DOI：
10.1152/ajprenal.1985.249.1.f20
发表时间：
1985
期刊：
The American journal of physiology
影响因子：
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作者：
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DOI：
10.1172/jci111925
发表时间：
1985
期刊：
The Journal of clinical investigation
影响因子：
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作者：
Schuster,VL
通讯作者：
Schuster,VL
DOI：
10.1152/ajprenal.1985.249.4.f546
发表时间：
1985
期刊：
The American journal of physiology
影响因子：
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作者：
Stetson,DL;Beauwens,R;Palmisano,J;Mitchell,PP;Steinmetz,PR
通讯作者：
Steinmetz,PR