Characterization of swelling-induced ion transport in HT-29Cl.19A cells. Role of inorganic and organic osmolytes during regulatory volume decrease

1996 ◽  
Vol 433 (3) ◽  
pp. 276-286 ◽  
Author(s):  
R. B. Bajnath ◽  
H. R. de Jonge ◽  
A. J. Borgdorff ◽  
M. Zuiderwijk ◽  
J. A. Groot
Keyword(s):  
Ion Transport ◽  
Regulatory Volume Decrease ◽  
Organic Osmolytes ◽  
Volume Decrease ◽  
Inorganic And Organic

Regulatory volume decrease after swelling induced by urea in fibroblasts: prominent role of organic osmolytes

2007 ◽  
Vol 306 (1-2) ◽  
pp. 95-104 ◽  
Author(s):  
Alejandra López-Domínguez ◽  
Gerardo Ramos-Mandujano ◽  
Erika Vázquez-Juárez ◽  
Herminia Pasantes-Morales
Keyword(s):  
Regulatory Volume Decrease ◽  
Organic Osmolytes ◽  
Volume Decrease

Volume-activated K+ and Cl- pathways of dissociated epithelial cells (MDCK): role of Ca2+

1990 ◽  
Vol 258 (5) ◽  
pp. C827-C834 ◽  
Author(s):  
A. Rothstein ◽  
E. Mack
Keyword(s):  
Mdck Cells ◽  
Regulatory Volume Decrease ◽  
Disulfonic Acid ◽  
Ionophore A23187 ◽  
Madin Darby Canine Kidney ◽  
Osmotic Swelling ◽  
Volume Activation ◽  
Darby Canine Kidney ◽  
Volume Decrease

Osmotic swelling of dissociated Madin-Darby canine kidney (MDCK) cells in NaCl medium is followed by shrinking (regulatory volume decrease, or RVD) or in KCl medium by secondary swelling. The cation ionophore gramicidin has little effect on volumes of isotonic cells but accelerates volume-activated changes in either medium. Immediately after hypotonic exposure, the membrane becomes transiently hyperpolarized followed by depolarization. The depolarization phase is diminished by the anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS). Swelling is also associated with an almost immediate increase in Ca2+ influx and elevation of cytoplasmic Ca2+ ([Ca2+]i) preceding RVD. In Ca2(+)-free medium, [Ca2+]i rapidly declines to a low level. Osmotic swelling, under these circumstances, is associated with a small transient increase in [Ca2+]i, but RVD or secondary swelling (in KCl) are minimal. Under these conditions, addition of gramicidin or the Ca2(+)-ionophore A23187 induces significant volume changes, although not as large as those found in the presence of Ca2+. Quinine inhibits RVD in the absence of gramicidin, but not in its presence; oligomycin C, DIDS, and trifluoperazine, on the other hand, inhibit in the presence of the ionophore. These findings suggest that in MDCK cells RVD involves activation of distinct conductive K+ and Cl- pathways which allow escape of KCl and osmotically obligated water and that activation of both pathways is associated with elevated [Ca2+]i derived largely from volume activation of a Ca2(+)-influx pathway.

Role of concentration and size of intracellular macromolecules in cell volume regulation

1997 ◽  
Vol 273 (2) ◽  
pp. C360-C370 ◽  
Author(s):  
J. C. Summers ◽  
L. Trais ◽  
R. Lajvardi ◽  
D. Hergan ◽  
R. Buechler ◽  
...  
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Molecular Physiology ◽  
Average Molecular Mass ◽  
Membrane Stretch ◽  
Ca2 Channels ◽  
Volume Decrease

To gain insight into the mechanism(s) by which cells sense volume changes, specific predictions of the macromolecular crowding theory (A. P. Minton. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 181-190. A. P. Minton, C. C. Colclasure, and J. C. Parker. Proc. Natl. Acad. Sci. USA 89: 10504-10506, 1992) were tested on the volume of internally perfused barnacle muscle cells. This preparation was chosen because it allows assessment of the effect on cell volume of changes in the intracellular macromolecular concentration and size while maintaining constant the ionic strength, membrane stretch, and osmolality. The predictions tested were that isotonic replacement of large macromolecules by smaller ones should induce volume decreases proportional to the initial macromolecular concentration and size as well as to the magnitude of the concentration reduction. The experimental results were consistent with these predictions: isotonic replacement of proteins or polymers with sucrose induced volume reductions, but this effect was only observed when the replacement was > or = 25% and the particular macromolecule had an average molecular mass of < or = 20 kDa and a concentration of at least 18 mg/ml. Volume reduction was effected by a mechanism identical with that of hypotonicity-induced regulatory volume decrease, namely, activation of verapamil-sensitive Ca2+ channels.

Regulatory volume decrease in HL-60 cells: importance of rapid changes in permeability of Cl- and organic solutes

1994 ◽  
Vol 267 (4) ◽  
pp. C1045-C1056 ◽  
Author(s):  
K. R. Hallows ◽  
P. A. Knauf
Keyword(s):  
Regulatory Volume Decrease ◽  
Organic Osmolytes ◽  
Diffusion Kinetic ◽  
Nernst Potential ◽  
Ehrlich Ascites ◽  
Rapid Changes ◽  
36Cl Fluxes ◽  
Free Media ◽  
Rate Limiting ◽  
Volume Decrease

Results obtained through the use of inhibitors and isotope flux and equilibration techniques indicate that the regulatory volume decrease (RVD) response of human promyelocytic leukemic HL-60 cells occurs largely through the efflux of K+ and Cl- through separate conductive membrane pathways. These "channels" differ pharmacologically and in their modes of activation from those described in lymphocytes and Ehrlich ascites tumor cells. With use of measured 86Rb+ and 36Cl- fluxes, together with a diffusion kinetic model, the membrane potential (Em) and apparent K+ and Cl- permeabilities (PK and PCl) were estimated under various isotonic and hypotonic conditions. Under isotonic (300 mosM) conditions, Em is close to the Nernst potential for K+ and PCl is < 0.1 PK. Rapid and steeply graded increases in the measured Cl- efflux rate and calculated PCl occur with decreasing tonicity, with the largest increases at tonicities < 80% of isotonic. K+ efflux and the apparent PK increase only modestly with decreasing tonicity. At 50% tonicity, PCl rises to nearly 10 times PK, which should cause substantial membrane depolarization, with Em approaching the Nernst potential for Cl-. Gramicidin treatment markedly accelerates the rate of RVD and net 36Cl- efflux in hypotonic Na(+)-and Cl(-)-free media, providing further evidence that PK is rate limiting during RVD. K+ loss exceeds Cl- loss during RVD, and the total loss of K+ and Cl- is insufficient to account for the observed degree of volume recovery in 50% tonicity media, indicating that other (organic) osmolytes must take part in the HL-60 cell RVD response.

CFTR-dependent and -independent swelling-activated K+ currents in primary cultures of mouse nephron

2003 ◽  
Vol 284 (4) ◽  
pp. F812-F828 ◽  
Author(s):  
Radia Belfodil ◽  
Hervé Barrière ◽  
Isabelle Rubera ◽  
Michel Tauc ◽  
Chantal Poujeol ◽  
...  
Keyword(s):  
Primary Cultures ◽  
Regulatory Volume Decrease ◽  
Mouse Kidney ◽  
Wild Type ◽  
Collecting Tubule ◽  
K Currents ◽  
Volume Decrease ◽  
Autocrine Mechanism ◽  
Cortical Collecting Tubule

The role of CFTR in the control of K+ currents was studied in mouse kidney. Whole cell clamp was used to identify K+ currents on the basis of pharmacological sensitivities in primary cultures of proximal (PCT) and distal convoluted tubule (DCT) and cortical collecting tubule (CCT) from wild-type (WT) and CFTR knockout (KO) mice. In DCT and CCT cells, forskolin activated a 293B-sensitive K+ current in WT, but not in KO, mice. In these cells, a hypotonic shock induced K+ currents blocked by charybdotoxin in WT, but not in KO, mice. In PCT cells from WT and KO mice, the hypotonicity-induced K+ currents were insensitive to these toxins and were activated at extracellular pH 8.0 and inhibited at pH 6.0, suggesting that the corresponding channel was TASK2. In conclusion, CFTR is implicated in the control of KCNQ1 and Ca2+-sensitive swelling-activated K+ conductances in DCT and CCT, but not in proximal convoluted tubule, cells. In KO mice, impairment of the regulatory volume decrease process in DCT and CCT could be due to the loss of an autocrine mechanism, implicating ATP and adenosine, which controls swelling-activated Cl− and K+channels.

Mechanisms of regulatory volume decrease in UC-11MG human astrocytoma cells

1993 ◽  
Vol 264 (5) ◽  
pp. C1201-C1209 ◽  
Author(s):  
S. Medrano ◽  
E. Gruenstein
Keyword(s):  
Brain Injuries ◽  
Regulatory Volume Decrease ◽  
Transport Pathways ◽  
Astrocytoma Cells ◽  
Hypotonic Treatment ◽  
Human Astrocytoma ◽  
Stretch Activated Channels ◽  
Human Astrocytoma Cells ◽  
Volume Decrease

Swelling of astrocytes commonly occurs after cerebral ischemia and other brain injuries. Because these cells constitute 20-25% of human brain volume, their swelling is a major factor in the morbidity and mortality associated with cerebral edema. Many cells, including astrocytes, resist or reverse the tendency to swell by activating transport pathways that lead to a regulatory volume decrease. Here we report the results of studies designed to elucidate the mechanisms of the regulatory volume decrease that occurs after astrocytes are swollen by exposure to hypotonic medium. Using UC-11MG cells, a well-characterized, human, astrocytoma-derived line, we observed an increase in membrane permeability to both K+ and Cl- during regulatory volume decrease, consistent with a net loss of these ions. Neither the increase in K+ exit nor the regulatory volume decrease was affected by bumetanide, an inhibitor of anion-cation cotransport. On the other hand, the increased K+ efflux, as well as the regulatory volume decrease, was blocked by Gd3+, suggesting a putative role of stretch-activated cationic channels in the process of volume regulation. Although increases in intracellular free Ca2+ were also observed during hypotonic treatment, they occurred well after the onset of the regulatory volume decrease. Furthermore, the regulatory volume decrease was not affected by blocking the intracellular free Ca2+ increase with dimethyl 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid or by removal of extracellular Ca2+. These results indicate that the regulatory volume decrease in UC-11MG cells may involve stretch-activated channels that operate independently of changes in intracellular free Ca2+.

Cation transport in mouse erythrocytes: role of K(+)-Cl- cotransport in regulatory volume decrease

1995 ◽  
Vol 268 (4) ◽  
pp. C894-C902 ◽  
Author(s):  
C. C. Armsby ◽  
C. Brugnara ◽  
S. L. Alper
Keyword(s):  
Volume Regulation ◽  
Inhibitory Concentration ◽  
Inbred Mouse ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Cation Transport ◽  
Hypotonic Medium ◽  
Hypotonic Swelling ◽  
Volume Decrease

We investigated cation transport and cell volume regulation in erythrocytes of CD1 and C57/B6 mice. Swelling of cells from either strain stimulated K+ efflux that was insensitive to ouabain, bumetanide, and clotrimazole. Seventy-five percent of swelling-induced K+ efflux was Cl- dependent (inhibited by sulfamate or methanesulfonate, partially by NO3-, but not by SCN-) and was inhibited by okadaic acid (OA; 50% inhibitory concentration = 18 +/- 6 nM in CD1 and 10 +/- 4 nM in C57/B6). In both strains, K+ efflux into isotonic medium was stimulated by staurosporine or by N-ethylmaleimide, and the latter was partially blocked by pretreatment of cells with OA. When cells of either strain were incubated in hypotonic medium or preswollen isosmotically with nystatin, OA-sensitive regulatory volume decrease (RVD) and K+ loss were observed. RVD produced by hypotonic swelling was prevented by Cl- replacement with sulfamate or methanesulfonate. These properties suggest the presence in outbred and inbred mouse erythrocytes of RVD mediated by K(+)-Cl- cotransport.

scholarly journals Regulatory volume decrease in cultured kidney cells (A6): role of amino acids.

1995 ◽  
Vol 106 (3) ◽  
pp. 525-542 ◽  
Author(s):  
P De Smet ◽  
J Simaels ◽  
P E Declercq ◽  
W Van Driessche
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Acid Concentration ◽  
Short Circuit ◽  
Regulatory Volume Decrease ◽  
Short Circuit Current ◽  
Amino Acid Concentration ◽  
Cell Content ◽  
Volume Decrease

Volume regulation was studied in A6 epithelia grown on permeable supports by measuring cell thickness (Tc) while simultaneously recording short circuit current (ISC) and transepithelial conductance (Gt). Lowering the tonicity of the basolateral solution (pi b) from 250 or 215 to 140 mOsm/kg elicited a rapid rise in Tc followed by a regulation of the cell volume towards control. This decrease in Tc displays the characteristics of the regulatory volume decrease (RVD). Upon restoring the isoosmotic conditions, Tc decreased rapidly below its control value. A post RVD regulatory volume increase (RVI) as described for other cell types was not observed. The subsequent reduction of the basolateral osmolality increased Tc to the level recorded at the end of the first hypoosmotic pulse. Because cell content was not altered during the isoosmotic period the second hypoosmotic challenge was isotonic with the cell and did therefore not evoke an RVD. However, the cell did not lose its ability to volume regulate since an RVD could be elicited by further reduction of pi b from 140 to 100 mOsm/kg. The possibility of an involvement of amino acids in the RVD was tested. The amount of amino acids in the cell as well as excreted in the bath was determined by amino acid analysis. Millimolar concentrations of threonine, serine, alanine, glutamate, glycine and aspartate were found in the cell extract. The cellular amino acid concentration was 28.8 +/- 0.4 mM. The amounts of glycine, aspartate and glutamate excreted from the cell during the hypotonic treatment were significantly larger than in control conditions. The excretion of these amino acids during hypotonicity decreased the cellular amino acid concentration by 8.4 +/- 0.2 mM. This quantity cannot completely account for the RVD during the first hypotonic challenge. The addition of glycine, aspartate and glutamate to the bathing solutions, although used at concentrations higher than intracellularly, did not reduce RVD. On the contrary, this maneuver increased the amplitude of the RVD following both hypoosmotic pulses. This result suggests a stimulatory role of the amino acids on the processes responsible for the RVD.

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