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Journal articles on the topic 'Hypotonic shock'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

Dinh, Xuan Tu, Huynh Thi Diem Suong Le, and Minh Ly Nguyen. "The chromosome numbers of Panax vietnamensis Ha et Grushv." Can Tho University Journal of Science 14, CBA (October 27, 2022): 86–90. http://dx.doi.org/10.22144/ctu.jen.2022.033.

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The somatic chromosome number of Panax vietnamensis Ha et Grushv. was determined to be 2n = 24, based on the hypotonic shock method by potassium chloride solution. In this study, we investigated the effect of potassium chloride and colchicine solutions on chromosome dispersion of Panax vietnamensis at different concentrations. The treatment using 0.2% KCl solution in 45 minutes combined with 0.05% colchicine solution in 2 hours subsequently resulted in proper hypotonia. The result showed that chromosomes were evenly dispersed. The hypotonic shock method seemed to be effective in equally distributing chromosomes. The result can be applied in cell genetic studies and selective breeding programs for Panax vietnamensis.
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2

Beck, J. S., S. Breton, G. Giebisch, and R. Laprade. "Potassium conductance regulation by pH during volume regulation in rabbit proximal convoluted tubules." American Journal of Physiology-Renal Physiology 263, no. 3 (September 1, 1992): F453—F458. http://dx.doi.org/10.1152/ajprenal.1992.263.3.f453.

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When rabbit proximal convoluted tubules were microperfused in the presence of bicarbonate, a 90 mosmol hypotonic shock hyperpolarized the basolateral membrane by 5.5 +/- 1.4 mV, increased basolateral potassium selectivity (tK) from 0.30 +/- 0.02 to 0.45 +/- 0.02, and reduced the basolateral membrane resistance from 4,887 +/- 821 to 2,836 +/- 602 omega.cm. These data show that the hypotonic shock increased absolute basolateral potassium conductance. The same hypotonic shock elevated intracellular pH from 7.18 +/- 0.04 to 7.31 +/- 0.04. When bath pH was increased by 0.2 pH units (by reduction of CO2), intracellular pH rose by 0.13 +/- 0.01. In separate experiments this maneuver hyperpolarized the basolateral membrane by 5.0 +/- 0.8 mV and augmented basolateral tK from 0.58 +/- 0.06 to 0.68 +/- 0.04, suggesting that the basolateral potassium conductance is sensitive to pH changes of a magnitude similar to that evoked by a hypotonic shock. In the nominal absence of bicarbonate or presence of 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS) in the bath, the hypotonic shock caused a transient intracellular acidification, suggesting involvement of basolateral bicarbonate transport in the hypotonic shock-induced alkalinization. In the absence of bicarbonate, the hypotonic shock did not increase basolateral tK or induce hyperpolarization of the basolateral membrane. We conclude that the increase in potassium conductance observed during hypotonic shock is at least partly mediated by a bicarbonate-dependent, SITS-sensitive intracellular alkalinization.
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3

Marshall, W. S., S. E. Bryson, and T. Luby. "Control of epithelial Cl(−) secretion by basolateral osmolality in the euryhaline teleost Fundulus heteroclitus." Journal of Experimental Biology 203, no. 12 (June 15, 2000): 1897–905. http://dx.doi.org/10.1242/jeb.203.12.1897.

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Euryhaline teleost fish adapt rapidly to salinity change and reduce their rate of ion secretion on entry to fresh water. Killifish (Fundulus heteroclitus) transferred from full-strength sea water to fresh water showed large reductions in plasma [Na(+)] and osmolality at 6 h which were corrected by 24 h. To mimic this in vitro, a hypotonic shock of 20–70 mosmol kg(−)(1) was applied on the basolateral side of opercular epithelia. This hypotonic shock reversibly reduced the short-circuit current (I(sc), equivalent to the rate of secretion of Cl(−)) in a dose-dependent fashion, with a 40 mosmol kg(−)(1) hypotonic shock reducing I(sc) by 58+/−4.6 % in 40 min. Similar reductions in [NaCl], but with added mannitol to maintain osmolality, were without effect, indicating that the effect was purely osmotic. Hypotonic inhibition of I(sc) was accompanied by reductions in epithelial conductance (G(t)) but no significant change in transepithelial potential (V(t)). The hypotonic inhibition was apparently not Ca(2+)-mediated because Ca(2+)-depleted salines, thapsigargin and ionomycin all failed to block the reduction in I(sc) produced by hypotonic shock. The inhibition was not mediated via a reduction in intracellular cyclic AMP level because cyclic AMP levels, measured by radioimmunoassay, were unchanged by hypotonic shock and by 1.0 micromol l(−)(1) clonidine (which inhibits I(sc) by changing intracellular [Ca(2+)]) but were increased markedly by 1.0 micromol l(−)(1) isoproterenol, a positive control. The protein tyrosine kinase inhibitor genistein (100 micromol l(−)(1)), but not its inactive analogue daidzein, inhibited I(sc) in normal osmolality but produced a stimulation of I(sc) after hypotonic shock (and after clonidine treatment). The inhibitory effects of genistein and hypotonicity were not additive, suggesting that the same portion of the I(sc) was inhibited by both treatments. These data are consistent with a model for Cl(−) transport regulation involving tyrosine phosphorylation in cell-swelling-induced inhibition of Cl(−) secretion when euryhaline teleosts adapt to fresh water.
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4

Bear, C. E. "A nonselective cation channel in rat liver cells is activated by membrane stretch." American Journal of Physiology-Cell Physiology 258, no. 3 (March 1, 1990): C421—C428. http://dx.doi.org/10.1152/ajpcell.1990.258.3.c421.

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A 16-pS channel was studied using patch-clamp electrophysiology in freshly dissociated rat liver cells and rat hepatoma cells. The channel was found to be cation selective and permeable to Na+, K+, and Ca2+. Its gating was unaffected by addition of the calcium ionophore A23187 (5 microM) in the presence of extracellular Ca2+ (2 mM). Ca2+ channel blockers, nifedipine, verapamil, and lanthanum, failed to inhibit the channel. The channel was activated by stretch, applied as suction to the interior of the patch pipette, and by cell swelling, induced by hypotonic shock or organic solute uptake (10 mM L-alanine). Channel activation by cell swelling was transient, lasting approximately 1 min. An elevation in cytosolic Ca2+ was evoked by hypotonic shock, as measured using the fluorescent indicator indo-1/AM. This change in intracellular Ca2+ concentration was dependent on extracellular Ca2+. Inasmuch as the time course for this response corresponded to that of channel activation, it is likely that hypotonic shock stimulated Ca2+ influx through the stretch-activated channel. To determine the role for Ca2+ influx in regulatory volume decrease (RVD), cell volume changes after hypotonic shock were studied using a Coulter counter. RVD was slightly but significantly inhibited by depletion of extracellular Ca2+. On the basis of these results it is proposed that stretch-activated channels in liver cells permit the transient influx of Ca2+, which in turn acts to trigger changes in ion conductance or cytoskeletal components involved in cell volume regulation.
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5

Fujii, Shuhei, and Johan A. Hellebust. "Release of intracellular glycerol and pore formation in Dunaliella tertiolecta exposed to hypotonic stress." Canadian Journal of Botany 70, no. 7 (July 1, 1992): 1313–18. http://dx.doi.org/10.1139/b92-164.

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When Dunaliella tertiolecta cells, previously cultured in a 0.5 M NaCl medium, were resuspended in a 0.25 NaCl medium, about 50% of the intracellular glycerol was lost within 2 min. A corresponding amount of glycerol appeared in the medium, while other organic solutes, such as amino acids and sugars, were not detected. These results indicate that intracellular glycerol is rapidly released without significant concomitant cell damage. Rubidum, in the case of rubidium-loaded cells, was also rapidly released to the medium in response to hypotonic shock. Gramicidin, dimers of which form stable membrane pores, caused rapid release of intracellular glycerol, while the ionophore, valinomycin, had no effect. When 0.5 M NaCl-grown cells were resuspended in 0.25 M NaCl medium, intracellular trapping of 14C-glycerol occurred but not of 14C-glucose, 14C-sucrose, or 14C-glycine. However, when 0.5 M NaCl-grown cells were resuspended in 0.05 M NaCl medium, intracellular trapping of small amounts of, 14C-glucose, 14C-sucrose, or 14C-glycine, in addition to considerable amounts of 14C-glycerol, occurred. These results indicate that abrupt hypotonic shocks cause transient formation of small nonspecific pores in the plasma membrane of D. tertiolecta cells and that intracellular glycerol is released to the medium through such nonspecific transient pores. Key words: Dunaliella, hypotonic shock, glycerol release, rubidum, pore formation.
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6

Macri, P., S. Breton, J. S. Beck, J. Cardinal, and R. Laprade. "Basolateral K+, Cl-, and HCO3- conductances and cell volume regulation in rabbit PCT." American Journal of Physiology-Renal Physiology 264, no. 2 (February 1, 1993): F365—F376. http://dx.doi.org/10.1152/ajprenal.1993.264.2.f365.

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The relationship between changes in cellular volume, intracellular pH (pHi), basolateral membrane potential (VBL), and membrane partial basolateral conductances to K+ (tK) and Cl- (tCl) and mediated by the Na-HCO3 cotransporter (tNaHCO3) was determined in the collapsed proximal convoluted tubule (PCT) submitted to a 125-mosmol/kg hypotonic shock. The shock that produces a rapid swelling followed by partial volume regulation was accompanied by a rapid and transient VBL hyperpolarization of 10.0 +/- 1.5 mV and a second gradual hyperpolarization of 5.0 +/- 0.7 mV with respect to a control value of -44.0 +/- 4.6 mV.tK was 0.12 +/- 0.03 in control, increased transiently to 0.15 +/- 0.03, and then gradually increased to reach 0.32 +/- 0.06 at the end of hypotonic shock. In contrast, tCl was 0.03 +/- 0.01 in control, increased rapidly to a maximum of 0.16 +/- 0.01, and then decreased slowly to 0.08 +/- 0.02. During the same period, tNaHCO3 decreased rapidly from 0.41 +/- 0.04 to a minimum of 0.11 +/- 0.02 and slowly reincreased to reach 0.16 +/- 0.01.pHi increased transiently from 7.09 +/- 0.03 in control to 7.24 +/- 0.05 to come back gradually to 7.15 +/- 0.05 at the end of the hypotonic period. The membrane absolute conductance mediated by the Na-HCO3 cotransporter was found to increase only slightly in hypotonic conditions, whereas that to K+ and Cl-, GK and GCl, increased by at least factors of 8 and 17, respectively, with the increase of GCl being much faster than that of GK. In addition, the temporal variations in GCl followed closely those of the cellular water efflux. We conclude that the hypotonic swelling leads to important increases in the conductive pathways for K+ and Cl- and that the Cl- conductance pathway appears to be the rate limiting step in triggering and supporting regulatory volume decrease.
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7

Batiza, Ann F., Tara Schulz, and Patrick H. Masson. "Yeast Respond to Hypotonic Shock with a Calcium Pulse." Journal of Biological Chemistry 271, no. 38 (September 20, 1996): 23357–62. http://dx.doi.org/10.1074/jbc.271.38.23357.

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8

Galietta, L. J., S. Falzoni, F. Di Virgilio, G. Romeo, and O. Zegarra-Moran. "Characterization of volume-sensitive taurine- and Cl(-)-permeable channels." American Journal of Physiology-Cell Physiology 273, no. 1 (July 1, 1997): C57—C66. http://dx.doi.org/10.1152/ajpcell.1997.273.1.c57.

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Volume-sensitive Cl- channels [ICl(vol)] were studied using taurine efflux and patch-clamp experiments in 9HTEo- human tracheal cells. Cells were stimulated with the Ca(2+)- elevating agents ATP and ionomycin in isotonic medium or in hypotonic solutions. ATP (100 microM) or ionomycin (1 microM) and hypotonic shock produced a synergic effect. Indeed, the resulting taurine efflux was much higher than the sum of the single effects elicited by ATP, ionomycin, or hypotonic medium. The taurine release elicited by hypotonic shock and the potentiation by ATP and ionomycin were markedly inhibited by using a Ca(2+)-free extracellular medium and by incubating the cells with the membrane-permeable 1,2-bis(2-amino- phenoxy)ethane-N,N,N',N'-tetraacetic acid acetoxymethyl ester chelating agent. Patch-clamp experiments confirmed the role of Ca2+ on ICl(vol) channels. Swelling-induced taurine efflux was inhibited by reactive blue 2, suramin, and pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid. Patch-clamp experiments demonstrated that these compounds shift the voltage-dependent inactivation of ICl(vol) channels toward more negative values. This study indicates that the sensitivity of ICl(vol) to cell volume changes is modulated by intracellular Ca2+ and that purinergic receptor antagonists represent a new class of CI- channel blockers.
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9

Smets, Ilse, Marcel Ameloot, Paul Steels, and Willy Van Driessche. "Loss of cell volume regulation during metabolic inhibition in renal epithelial cells (A6): role of intracellular pH." American Journal of Physiology-Cell Physiology 283, no. 2 (August 1, 2002): C535—C544. http://dx.doi.org/10.1152/ajpcell.00371.2001.

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In renal ischemia, tubular obstruction induced by swelling of epithelial cells might be an important mechanism for reduction of the glomerular filtration rate. We investigated ischemic cell swelling by examining volume regulation of A6 cells during metabolic inhibition (MI) induced by cyanide and 2-deoxyglucose. Changes in cell volume were monitored by recording cell thickness ( T c). Intracellular pH (pHc) measurements were performed with the pH-sensitive probe 5-chloromethyl-fluoresceine diacetate. T c measurements showed that MI increases cell volume. Cell swelling during MI is proportional to the rate of Na+ transport and is not followed by a volume regulatory response. Furthermore, MI prevents the regulatory volume decrease (RVD) elicited by a hyposmotic shock. MI induces a pronounced intracellular acidification that is conserved during a subsequent hypotonic shock. A transient acidification induced by a NH4Cl prepulse causes a marked delay of the RVD in response to a hypotonic shock. On the other hand, acute lowering of external pH to 5, simultaneously with the hypotonic shock, allowed the onset of RVD. However, this RVD was completely arrested ∼10 min after the initiation of the hyposmotic challenge. The inhibition of RVD appears to be related to the pronounced acidification that occurred within this time period. In contrast, when external pH was lowered 20 min before the hyposmotic shock, RVD was absent. These data suggest that internal acidification inhibits cellular volume regulation in A6 cells. Therefore, the intracellular acidification associated with MI might at least partly account for the failure of volume regulation in swollen epithelial cells.
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10

Dube, L., L. Parent, and R. Sauve. "Hypotonic shock activates a maxi K+ channel in primary cultured proximal tubule cells." American Journal of Physiology-Renal Physiology 259, no. 2 (August 1, 1990): F348—F356. http://dx.doi.org/10.1152/ajprenal.1990.259.2.f348.

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The nature and function of the ionic channels at the apical membrane of primary cultured proximal tubule cells (PT) was investigated by use of the extracellular patch-clamp method. Several types of ionic channels were observed, including a calcium-dependent K+ channel of 206 pS in symmetrical 162 mM KCl activated at depolarizing potentials [maxi K+(Ca2+)]. Whole cell experiments were also carried out that clearly indicated that the PT cells respond to a hypotonic shock by activating electroconductive pathways. This response consisted of an initial hyperpolarization (from -47 to -58 mV, SD = 3, n = 4), followed by a strong depolarization (to -23 mV, SD = 4, n = 4). Furthermore, it was found in cell-attached experiments that the maxi K+(Ca2+) channel becomes activated during the hypotonic challenge. The activation process required external Ca2+, although some residual single-channel activity was measured in the absence of extracellular calcium (n = 3). On the basis of these results, it is concluded that the volume regulation process in PT cells in response to a hypotonic shock involves an influx of calcium from the external medium, which in turn triggers the opening of apical maxi K+(Ca2+) channels.
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11

Shpakova, Natalia, and Natalia Orlova. "About the Mechanism of Mammalian Erythrocytes Osmotic Stability." Problems of Cryobiology and Cryomedicine 30, no. 4 (December 17, 2020): 331–42. http://dx.doi.org/10.15407/cryo30.04.331.

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The peculiarities of the effect of hypertonic shock and hypotonic stress on erythrocytes of different species of mammals (human, bull, horse, rabbit, dog, rat) have been investigated. Based on the results of correlation analysis (using the Spearman’s rank correlation coefficient), the relationship between osmotic sensitivity of mammalian erythrocytes and the well-known structural and functional characteristics of these cells was assessed. The paper presents and analyzes the significant relationships. Under hypotonic stress of mammalian erythrocytes, the values of the threshold concentration of NaCl and the one of osmotic fragility were found to correlate with the size of cells (diameter). Under hypertonic shock of mammalian erythrocytes, the values of the threshold concentrations of NaCl and that of hemolysis of cells in a medium containing 4.0 mol/L NaCl correlated with the membrane permeability to water. Mammalian erythrocytes with a high value of the coefficient of diffusion water transport due to the protein channels are more resistant to hypertensive shock.
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12

Huang, L. E., L. Caruccio, A. Y. Liu, and K. Y. Chen. "Rapid activation of the heat shock transcription factor, HSF1, by hypo-osmotic stress in mammalian cells." Biochemical Journal 307, no. 2 (April 15, 1995): 347–52. http://dx.doi.org/10.1042/bj3070347.

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Osmoregulation is important to living organisms for survival in responding to environmental changes of water and ionic strength. We demonstrated here for the first time that exposure of HeLa cells to a hypotonic medium (30% growth medium and 70% water) prominently induced the binding activity of the heat shock transcription factor (HSF). Pretreatment of cells with cycloheximide did not inhibit the induction of HSF-binding activity, indicating that the mechanisms of induction are independent of new protein synthesis. The magnitude of hypo-osmotic stress-induced HSF-binding activity was comparable with that induced by heat shock. The induction, as monitored by gel-mobility-shift assay, occurred within 5 min of hypo-osmotic stress and persisted at least up to 4 h in HeLa cells under the hypotonic conditions. Addition of sorbitol to the hypotonic medium abolished HSF activation. Hypo-osmotic stress-induced HSF binding could also be demonstrated in HeLa cells maintained in simple sorbitol solution by decreasing the sorbitol concentration from 300 mM to 200 mM or less. Competition analysis suggests that the effects of hypo-osmotic stress on HSF-binding activity was specific. Cross-linking experiments and Western-blot analysis demonstrated that hypo-osmotic stress induced trimerization of human heat shock factor 1 (HSF1) in intact HeLa cells, suggesting that trimer formation of HSF1 was responsible for inducing HSF-binding activity in hypo-osmotically stressed cells. However, unlike heat shock response, the activation of HSF by hypo-osmotic stress did not lead to accumulation of hsp70 mRNA in HeLa cells.
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13

Duranton, C., E. Mikulovic, M. Tauc, M. Avella, and P. Poujeol. "Potassium channels in primary cultures of seawater fish gill cells. II. Channel activation by hypotonic shock." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 5 (November 1, 2000): R1659—R1670. http://dx.doi.org/10.1152/ajpregu.2000.279.5.r1659.

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Previous studies performed on apical membranes of seawater fish gills in primary culture have demonstrated the existence of stretch-activated K+channels with a conductance of 122 pS. The present report examines the involvement of K+ channels in ion transport mechanisms and cell swelling. In the whole cell patch-clamp configuration, K+ currents were produced by exposing cells to a hypotonic solution or to 1 μM ionomycin. These K+ currents were inhibited by the addition of quinidine and charybdotoxin to the bath solution. Isotopic efflux measurements were performed on cells grown on permeable supports using 86Rb+ as a tracer to indicate potassium movements. Apical and basolateral membrane86Rb effluxes were stimulated by the exposure of cells to a hypotonic medium. During the hypotonic shock, the stimulation of86Rb efflux on the apical side of the monolayer was inhibited by 500 μM quinidine or 100 μM gadolinium but was insensitive to scorpion venom [ Leirus quinquestriatus hebraeus (LQH)]. An increased 86Rb efflux across the basolateral membrane was also reduced by the addition of quinidine and LQH venom but was not modified by gadolinium. Moreover, basolateral and apical membrane 86Rb effluxes were not modified by bumetanide or thapsigargin. There is convincing evidence for two different populations of K+ channels activated by hypotonic shock. These populations can be separated according to their cellular localization (apical or basolateral membrane) and as a function of their kinetic behavior and pharmacology.
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14

Breton, S., M. Marsolais, J. Y. Lapointe, and R. Laprade. "Cell volume increases of physiologic amplitude activate basolateral K and CI conductances in the rabbit proximal convoluted tubule." Journal of the American Society of Nephrology 7, no. 10 (October 1996): 2072–87. http://dx.doi.org/10.1681/asn.v7102072.

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The effects of increases in cell volume (CV) of physiologic amplitude, induced either hypotonically or isotonically, were studied on the three major basolateral conductances of rabbit isolated proximal convoluted tubules. CV increases were produced by a 40 mosmol/kg H2O hypotonic shock or by the isotonic replacement of mannitol by 40 mM glucose or alanine. The hypotonic shock led to an increase in CV of 17 +/- 3% (N = 8), whereas additions of glucose and alanine led to increases in CV of 22.6 +/- 2.5% (N = 7) and 28.3 +/- 3.5 (N = 5), respectively. Under all of these conditions, the absolute conductance mediated by the NaHCO3 cotransporter did not vary appreciably. This allowed determination of the variations of the absolute conductances to potassium (GK) and chloride (GCl) from their measured partial conductances. All three protocols induced significant increases in GK by factors of 2.37 +/- 0.3, 1.43 +/- 0.16, and 1.69 +/- 0.40, and in GCI by factors of 3.32 +/- 0.57, 3.68 +/- 0.75, and 3.90 +/- 1.0 during the hypotonic, glucose, and alanine protocols, respectively. These increases in GK and GCl occurred with a delay compared with the variations in CV, indicating a more elaborate signaling mechanism than stretch-activation of channels that are known to activate channels within seconds. Intracellular pH increased from 7.19 +/- 0.03 to 7.23 +/- 0.03, 7.17 +/- 0.02 to 7.20 +/- 0.02, and 7.13 +/- 0.01 to 7.16 +/- 0.01 after the hypotonic shock and the glucose and alanine additions, respectively. The study presented here demonstrates that there is a close relationship between CV and GK and GCl, independent of the means used (hypotonically or isotonically) to increase CV in rabbit proximal convoluted tubules. CV activation of GK is proposed to account for part of the increase in GK reported previously during activation of transepithelial transport.
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15

Cutler, Adrian J., and Mohammed Saleem. "Permeabilizing Soybean Protoplasts to Macromolecules Using Electroporation and Hypotonic Shock." Plant Physiology 83, no. 1 (January 1, 1987): 24–28. http://dx.doi.org/10.1104/pp.83.1.24.

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16

Rugolo, Michela, Teresa Mastocola, Alberto Flamigni, and Giorgio Lenaz. "Chloride transport in human fibroblasts is activated by hypotonic shock." Biochemical and Biophysical Research Communications 160, no. 3 (May 1989): 1330–38. http://dx.doi.org/10.1016/s0006-291x(89)80149-4.

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17

Mastrocola, Teresa, Alberto Flamigni, and Michela Rugolo. "Hypotonic shock activated Cl− and K+ pathways in human fibroblasts." Biochimica et Biophysica Acta (BBA) - Biomembranes 1069, no. 2 (November 1991): 201–8. http://dx.doi.org/10.1016/0005-2736(91)90125-r.

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18

Bianchini, L., B. Fossat, J. Porthe-Nibelle, J. C. Ellory, and B. Lahlou. "Effects of hyposmotic shock on ion fluxes in isolated trout hepatocytes." Journal of Experimental Biology 137, no. 1 (July 1, 1988): 303–18. http://dx.doi.org/10.1242/jeb.137.1.303.

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Isolated trout hepatocytes exposed to hypotonic Hank's medium (isotonicity × 0.70) swelled to 1.17 times the control volume after 3 min; by 15 min the cell volume had returned to normal. The ouabain-insensitive K+ uptake increased, indicating an immediate rise in K+ membrane permeability. As indicated by analysis of cellular contents, the regulatory volume decrease (RVD) was ensured by a release of intracellular K+. Na+ was not implicated in this mechanism. This potassium permeability induced by hypotonic shock was transient (maximum at 6 min), insensitive to blocking agents of voltage- and Ca2+-dependent K+ channels, and chloride-dependent. This result, together with a time-course of Cl- uptake similar to that of K+, suggests a K+/Cl- cotransport mechanism. This cotransport is inhibited by high furosemide concentrations (10(−3) mol l-1) but not by bumetanide (10(−4) mol l-1) or piretanide (10(−4) mol l-1).
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19

Leeson, Cale E., Brianna-Lee Beaudry, and Geoffrey R. Wignall. "Septic Shock Immediately following Percutaneous Suprapubic Catheterization." Case Reports in Urology 2021 (August 31, 2021): 1–3. http://dx.doi.org/10.1155/2021/2184866.

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Suprapubic catheterization (SPC) is considered a safe and effective procedure for long-term bladder decompression. With proper technique and appropriate patient selection, significant complications of SPC are rare. Immediate postoperative septic shock (i.e., within the first 24 hours of surgery) is rarely reported. We report a case of an 83-year-old patient who developed septic shock within one hour of suprapubic catheterization for a chronic hypotonic bladder, highlighting the importance of early recognition of complications from SPC and prompt management to ensure positive outcomes.
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20

Zhang, Zheng, and David M. Cohen. "Hypotonicity increases transcription, expression, and action ofEgr-1in murine renal medullary mIMCD3 cells." American Journal of Physiology-Renal Physiology 273, no. 5 (November 1, 1997): F837—F842. http://dx.doi.org/10.1152/ajprenal.1997.273.5.f837.

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In cells of the murine renal inner medullary collecting duct (mIMCD3) cell line, acute hypotonic shock (50% dilution of medium with sterile water but not with sterile 150 mM NaCl) increased Egr-1 mRNA abundance 2.5-fold at 6 h, as determined by Northern analysis. This increase was accompanied by increased Egr-1 transcription, as quantitated by luciferase reporter gene assay. Increased transcription was dose dependent, additive with other Egr-1 transcriptional activators, and occurred in the absence of overt cytotoxicy, as quantitated via a fluorometric viability assay. In addition, hypotonic stress increased Egr-1 protein abundance, which was accompanied by augmented Egr-1-specific DNA binding ability, as measured via electrophoretic mobility shift assay. Increased DNA binding was further associated with increased transactivation by Egr-1, demonstrated through transient transfection of mIMCD3 cells with a luciferase reporter gene driven by tandem repeats of the Egr-1 DNA consensus sequence. Taken together, these data indicate that hypotonic stress activates Egr-1 transcription, translation, DNA binding, and transactivation in renal medullary cells. This phenomenon might play a role in the acquisition of the adaptive phenotype in response to hypotonic stress in cells of the renal medulla in vivo.
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21

WILKINS, R. J., T. P. AFAIRFAX, M. E. DAVIES, M. C. MUZYAMBA, and J. S. GIBSON. "Homeostasis of intracellular Ca2+ in equine chondrocytes: response to hypotonic shock." Equine Veterinary Journal 35, no. 5 (January 5, 2010): 439–43. http://dx.doi.org/10.2746/042516403775600541.

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22

Sánchez, J. C., and R. J. Wilkins. "Effects of hypotonic shock on intracellular pH in bovine articular chondrocytes." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 135, no. 4 (August 2003): 575–83. http://dx.doi.org/10.1016/s1095-6433(03)00138-7.

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23

Straub, Susanne G., Samira Daniel, and Geoffrey W. G. Sharp. "Hyposmotic shock stimulates insulin secretion by two distinct mechanisms. Studies with the βHC9 cell." American Journal of Physiology-Endocrinology and Metabolism 282, no. 5 (May 1, 2002): E1070—E1076. http://dx.doi.org/10.1152/ajpendo.00176.2001.

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Exposure of βHC9 cells to a Krebs-Ringer bicarbonate-HEPES buffer (KRBH) made hypotonic by a reduction of 25 mM NaCl resulted in a prompt stimulation of insulin release. The stimulation was transient, and release rates returned to basal levels after 10 min. The response resembles that of the first phase of glucose-stimulated insulin release. The response did not occur if the reduction in NaCl was compensated for by the addition of an equivalent osmolar amount of sorbitol, so the stimulation of release was due to the osmolarity change and not the reduction in NaCl. The hyposmotic shock released insulin in KRBH with or without Ca2+. The L-type Ca2+ channel blocker nitrendipine inhibited the response in normal KRBH but had no effect in KRBH without Ca2+ despite the latter response being larger than in the presence of extracellular Ca2+. Similar data were obtained with calciseptine, which also blocks L-type channels. The T-type Ca2+ channel blocker flunarizine was without effect, as was the chloride channel blocker DIDS. In parallel studies, the readily releasable pool of insulin-containing granules was monitored. Immunoprecipitation of the target-SNARE protein syntaxin and co-immunoprecipitation of the vesicle-SNARE VAMP-2 was used as an indicator of the readily releasable granule pool. After hypotonic shock in the presence of extracellular Ca2+, the amount of VAMP-2 coimmunoprecipitated by antibodies against syntaxin was much reduced compared with controls. Therefore, under these conditions, hypotonic shock stimulates exocytosis of the readily releasable pool of insulin-containing granules. No such reduction was seen in the absence of extracellular Ca2+. In conclusion, after reexamination of the effect of hyposmotic shock on insulin secretion in the presence and absence of Ca2+ (with EGTA in the medium), it is clear that two different mechanisms are operative under these conditions. Moreover, these two mechanisms may be associated with the release of two distinct pools of insulin-containing granules.
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24

Daborn, K., R. R. F. Cozzi, and W. S. Marshall. "Dynamics of Pavement Cell–Chloride Cell Interactions During Abrupt Salinity Change in FUNDULUS HETEROCLITUS." Journal of Experimental Biology 204, no. 11 (June 1, 2001): 1889–99. http://dx.doi.org/10.1242/jeb.204.11.1889.

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SUMMARY Freshwater-adapted killifish (Fundulus heteroclitus) opercular epithelia were dissected and subjected to blood-side hypertonic bathing solution in Ussing-style chambers to simulate the increase in blood osmolality during migration to sea water. Conversely, seawater-acclimated killifish opercular epithelia were subjected to hypotonic bathing solutions to simulate the initial stages of migration to fresh water. Freshwater-acclimation (hypertonic stress) induced a rapid (approximately 30min) increase in membrane conductance (Gt) from 3.10±0.56 to 7.52±1.15mScm−2 (P<0.01, N=27), whereas seawater-acclimation (hypotonic stress) induced a rapid decrease in Gt from 8.22±1.15 to 4.41±1.00mScm−2 (P<0.01, N=27; means ± s.e.m.). Control seawater-acclimated membranes had a density of apical crypts (where chloride cells are exposed to the environment; detected by scanning electron microscopy) of 1133±96.4cryptsmm−2 (N=12), whereas the hypotonically shocked specimens had a lower crypt density of 870±36.7cryptsmm−2 (P<0.01 N=10; means ± s.e.m.). Hypertonic shock of freshwater membranes increased crypt density from 383.3±73.9 (N=12) to 630±102.9cryptsmm−2 (P<0.05; N=11; means ± s.e.m.). There was no change in density of chloride cells, as detected by fluorescence microscopy; hence, osmotic stress changes the degree of exposure, not the number of chloride cells. Cytochalasin D (5.0μmoll−1) completely blocked the conductance response to hypotonic shock and the reduction in apical crypt density measured by scanning electron microscopy, while phalloidin (33μmoll−1), colchicine (3×10−4moll−1) and griseofulvin (1.0μmoll−1) were ineffective. Actin imaging by phalloidin staining and confocal microscopy revealed extensive actin cords in pavement cell microridges and a ring of actin at the apex of chloride cells. We conclude that the actin cytoskeleton of chloride cells is required to maintain crypt opening and that osmotic shock causes chloride cells to adjust their apical crypt size.
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25

Rubera, Isabelle, Hervé Barrière, Michel Tauc, Michel Bidet, Catherine Verheecke-Mauze, Chantal Poujeol, Béatrice Cuiller, and Philippe Poujeol. "Extracellular adenosine modulates a volume-sensitive-like chloride conductance in immortalized rabbit DC1 cells." American Journal of Physiology-Renal Physiology 280, no. 1 (January 1, 2001): F126—F145. http://dx.doi.org/10.1152/ajprenal.2001.280.1.f126.

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Cl−currents induced by cell swelling were characterized in an immortalized cell line (DC1) derived from rabbit distal bright convoluted tubule by the whole cell patch-clamp techniques and by125I− efflux experiments. Exposure of cells to a hypotonic shock induced outwardly rectifying Cl−currents that could be blocked by 0.1 mM 5-nitro-2-(3-phenylpropyl-amino)benzoic acid, 1 mM DIDS, and by 1 mM diphenylamine-2-carboxylate. 125I− efflux experiments showed that exposure of the monolayer to a hypotonic medium increased 125I− loss. Preincubation of cells with LaCl3 or GdCl3 prevented the development of the response. The addition of 10 μM adenosine to the bath medium activated outwardly rectifying whole cell currents similar to those recorded after hypotonic shock. This conductance was inhibited by the A1-receptor antagonist 8-cyclopentyl-1,3-diproxylxanthine (DPCPX), LaCl3, or GdCl3 and was activated by GTPγS. The selective A1-receptor agonist N 6-cyclopentyladenosine (CPA) mimicked the effect of hypotonicity on 125I− efflux. The CPA-induced increase of 125I− efflux was inhibited by DPCPX and external application of LaCl3 or GdCl3. Adenosine also enhanced Mn2+ influx across the apical membrane. Overall, the data show that DC1 cells possess swelling- and adenosine-activated Cl− conductances that share identical characteristics. The activation of both conductances involved Ca2+ entry into the cell, probably via mechanosensitive Ca2+ channels. The effects of adenosine are mediated via A1 receptors that could mediate the purinergic regulation of the volume-sensitive Cl−conductance.
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26

Olmos, Gemma, L. Alfredo Lotero, M. Cristina Tejedor, and José C. Diez. "Delivery to Macrophages of Interleukin 3 Loaded in Mouse Erythrocytes." Bioscience Reports 20, no. 5 (October 1, 2000): 399–410. http://dx.doi.org/10.1023/a:1010334118492.

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Mouse carrier erythrocytes containing 125I-interleukin 3 have been prepared and treated with band 3 crosslinking reagents. The incorporation of interleukin 3 by hypotonic treatment into mouse erythrocytes reached levels of about 15% of the interleukin 3 added to the medium being predominantly present in the cytosolic fraction (73%). Uptake fell to about 7.4% when using the same conditions but omitting hypotonic shock. The interaction of band 3 crosslinked interleukin 3 loaded erythrocytes with macrophages was also studied. A high level of incorporation of interleukin 3 into macrophages was observed either from band 3 crosslinked, interleukin 3-loaded erythrocytes or from interleukin 3 loaded erythrocytes. The observations encourage the view that the system may be able to deliver and target cytokines and other growth factors to macrophages.
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27

Lemoine, J. L., R. Farley, and L. Huang. "Mechanism of efficient transfection of the nasal airway epithelium by hypotonic shock." Gene Therapy 12, no. 16 (May 12, 2005): 1275–82. http://dx.doi.org/10.1038/sj.gt.3302548.

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28

Schlotmann, R., F. Ch Mooren, R. Stoll, and W. Domschke. "Hypotonic shock causes an intracellular calcium increase in rat gastric parietal cells." Gastroenterology 108, no. 4 (April 1995): A214. http://dx.doi.org/10.1016/0016-5085(95)23517-5.

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29

McGrath, John J., and Peter C. Thomas. "The influence of osmotic species on human erythrocyte hypotonic cold shock hemolysis." Cryobiology 23, no. 6 (December 1986): 546. http://dx.doi.org/10.1016/0011-2240(86)90072-6.

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30

Faggio, Caterina, Agata Torre, Elisa Pelle, Federica Raffa, Valentina Villari, and Francesca Trischitta. "Cell volume regulation following hypotonic shock in hepatocytes isolated from Sparus aurata." Comparative Biochemistry and Physiology Part A: Molecular & Integrative Physiology 158, no. 1 (January 2011): 143–49. http://dx.doi.org/10.1016/j.cbpa.2010.10.002.

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31

Mignen, Olivier, Christelle Le Gall, Brian J. Harvey, and Serge Thomas. "Volume regulation following hypotonic shock in isolated crypts of mouse distal colon." Journal of Physiology 515, no. 2 (March 1999): 501–10. http://dx.doi.org/10.1111/j.1469-7793.1999.501ac.x.

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32

Pogorelov, A. G., and V. N. Pogorelova. "Dynamics of cell volume in early mouse embryos subjected to hypotonic shock." Biophysics 54, no. 3 (June 2009): 336–39. http://dx.doi.org/10.1134/s0006350909030130.

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33

Galizia, L., M. P. Flamenco, V. Rivarola, C. Capurro, and P. Ford. "Role of AQP2 in activation of calcium entry by hypotonicity: implications in cell volume regulation." American Journal of Physiology-Renal Physiology 294, no. 3 (March 2008): F582—F590. http://dx.doi.org/10.1152/ajprenal.00427.2007.

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We previously reported in a rat cortical collecting duct cell line (RCCD1) that the presence of aquaporin 2 (AQP2) in the cell membrane is critical for the rapid activation of regulatory volume decrease mechanisms (RVD) (Ford et al. Biol Cell 97: 687–697, 2005). The aim of our present work was to investigate the signaling pathway that links AQP2 to this rapid RVD activation. Since it has been previously described that hypotonic conditions induce intracellular calcium ([Ca2+]i) increases in different cell types, we tested the hypothesis that AQP2 could have a role in activation of calcium entry by hypotonicity and its implication in cell volume regulation. Using a fluorescent probe technique, we studied [Ca2+]i and cell volume changes in response to a hypotonic shock in WT-RCCD1 (not expressing aquaporins) and in AQP2-RCCD1 (transfected with AQP2) cells. We found that after a hypotonic shock only AQP2-RCCD1 cells exhibit a substantial increase in [Ca2+]i. This [Ca2+]i increase is strongly dependent on extracellular Ca2+ and is partially inhibited by thapsigargin (1 μM) indicating that the rise in [Ca2+]i reflects both influx from the extracellular medium and release from intracellular stores. Exposure of AQP2-RCCD1 cells to 100 μM gadolinium reduced the increase in [Ca2+]i suggesting the involvement of a mechanosensitive calcium channel. Furthermore, exposure of cells to all of the above described conditions impaired rapid RVD. We conclude that the expression of AQP2 in the cell membrane is critical to produce the increase in [Ca2+]i which is necessary to activate RVD in RCCD1 cells.
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34

Mitchell, C. H., J. J. Zhang, L. Wang, and T. J. Jacob. "Volume-sensitive chloride current in pigmented ciliary epithelial cells: role of phospholipases." American Journal of Physiology-Cell Physiology 272, no. 1 (January 1, 1997): C212—C222. http://dx.doi.org/10.1152/ajpcell.1997.272.1.c212.

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The whole cell recording technique was used to examine an outwardly rectifying chloride current activated by hypotonic shock in bovine pigmented ciliary epithelial (PCE) cells. Removal of internal and external Ca2+ did not affect the activation of these currents, but they were abolished by the phospholipase C inhibitor neomycin. The current was blocked by 5-nitro-2-(3-phenylpropylamino)benzoic acid, 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, and 4,4'-disothiocyanostilbene-2,2'-disulfonic acid (DIDS) in a voltage-dependent manner, but tamoxifen, dideoxyforskolin, and quinidine did not affect it. This blocking profile differs from that of the volume-sensitive chloride channel in neighboring nonpigmented ciliary epithelial cells (Wu, J., J. J. Zhang, H. Koppel, and T. J. C. Jacob, J. Physiol, Lond. 491: 743-755, 1996), and this difference implies that the volume responses of the two cell types are mediated by different chloride channels (Jacob, T. J. C., and J. J. Zhang. J. Physiol. Lond. In press). Intracellular administration of guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) to PCE cells induced a transient, time-independent, outwardly rectifying chloride current that closely resembled the current activated by hypotonic shock. DIDS produced a voltage-dependent block of the GTP gamma S-activated current similar to the block of the hypotonically activated current. Intracellular neomycin completely prevented activation of this current as did incubation of the cells in calphostin C. and inhibitor of protein kinase C (PKC). Removal of Ca2+ did not affect activation of the current by GTP gamma S but extended the duration of the response. Inhibition of phospholipase A2 (PLA2) with p-bromophenacyl bromide prevented the activation of the hypotonically induced current and also inhibited the current once activated by hypotonic solution. The findings imply that the hypotonic response in PCE cells is mediated by both phospholipase C (PLC) and PLA2. Both phospholipases generate arachidonic acid, and, in addition, the PLC pathway regulates the PLA2 pathway via a PKC-dependent phosphorylation of PLA2.
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35

Breton, S., J. S. Beck, J. Cardinal, G. Giebisch, and R. Laprade. "Involvement and source of calcium in volume regulatory decrease of collapsed proximal convoluted tubule." American Journal of Physiology-Renal Physiology 263, no. 4 (October 1, 1992): F656—F664. http://dx.doi.org/10.1152/ajprenal.1992.263.4.f656.

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We examined the role of Ca2+ in the volume regulatory decrease (VRD) of rabbit collapsed proximal tubules. Reduction of bath osmolality by 125 mosmol/kgH2O led to an initial cell swelling of 62.3 +/- 7.5% followed by a partial regulatory phase bringing cell volume to a value of 13.3 +/- 2.9% above control (n = 5). This swelling was accompanied by a transient intracellular Ca2+ ([Ca2+]i) increase from 174 +/- 33 to 306 +/- 67 nM (P < 0.05, n = 8). In the same condition, but in absence of extracellular Ca2+ ([Ca2+]e) [1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)], VRD following hypotonic shock was identical to that observed in presence of [Ca2+]e (n = 5), and [Ca2+]i increased transiently from 136 +/- 29 to 161 +/- 31 nM (P < 0.05, n = 5). Addition of 100 microM 8-(N,N-dimethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8), an agent known to inhibit Ca2+ release from intracellular stores, did not affect the initial cell swelling (63.4 +/- 4.2%), and VRD occurred to the same extent (25.0 +/- 7.1%, n = 4), although at a lower rate. In these conditions, [Ca2+]i, which was 113 +/- 30 nM in the isotonic solution, decreased progressively to 81 +/- 20 nM over the 5-min hypotonic period (n = 5). Mere preincubation with 100 microM TMB-8 before hypotonic shock led to a VRD identical to that observed in presence of Ca2+ and absence of TMB-8 while still blocking the Ca2+ release, with cell Ca2+ decreasing progressively from 179 +/- 32 to 87 +/- 21 nM (n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)
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36

Li, Jinqing, Patrick De Smet, Danny Jans, Jeannine Simaels, and Willy Van Driessche. "Swelling-activated cation-selective channels in A6 epithelia are permeable to large cations." American Journal of Physiology-Cell Physiology 275, no. 2 (August 1, 1998): C358—C366. http://dx.doi.org/10.1152/ajpcell.1998.275.2.c358.

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Effects of basolateral monovalent cation replacements (Na+ by Li+, K+, Cs+, methylammonium, and guanidinium) on permeability to86Rb of volume-sensitive cation channels (VSCC) in the basolateral membrane and on regulatory volume decrease (RVD), elicited by a hyposmotic shock, were studied in A6 epithelia in the absence of apical Na+ uptake. A complete and quick RVD occurred only when the cells were perfused with Na+ or Li+ saline. With both cations, hypotonicity increased basolateral86Rb release ([Formula: see text]), which reached a maximum after 15 min and declined back to control level. When the major cation was K+, Cs+, methylammonium, or guanidinium, the RVD was abolished. Methylammonium induced a biphasic time course of cell thickness (Tc), with an initial decline of Tc followed by a gradual increase. With K+, Cs+, or guanidinium, Tc increased monotonously after the rapid initial rise evoked by the hypotonic challenge. In the presence of K+, Cs+, or methylammonium,[Formula: see text] remained high during most of the hypotonic period, whereas with guanidinium blockage of[Formula: see text] was initiated after 6 min of hypotonicity, suggesting an intracellular location of the site of action. With all cations, 0.5 mM basolateral Gd3+ completely blocked RVD and fully abolished the [Formula: see text] increase induced by the hypotonic shock. The lanthanide also blocked the additional volume increase induced by Cs+, K+, guanidinium, or methylammonium. When pH was lowered from 7.4 to 6.0, RVD and[Formula: see text] were markedly inhibited. This study demonstrates that the VSCCs in the basolateral membrane of A6 cells are permeable to K+, Rb+, Cs+, methylammonium, and guanidinium, whereas a marked inhibitory effect is exerted by Gd3+, protons, and possibly intracellular guanidinium.
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37

LÖVKVIST WALLSTRÖM, Eva, Koichi TAKAO, Anna WENDT, Cristina VARGIU, Hong YIN, and Lo PERSSON. "Importance of the 3′ untranslated region of ornithine decarboxylase mRNA in the translational regulation of the enzyme." Biochemical Journal 356, no. 2 (May 24, 2001): 627–34. http://dx.doi.org/10.1042/bj3560627.

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Translational regulation of ornithine decarboxylase (ODC), which catalyses the first step in the biosynthesis of polyamines, appears to be an important mechanism in the strong feedback control as well as in the hypotonic induction of the enzyme. However, the exact mechanisms are not yet understood. The ODC mRNA has long 5′ and 3′ untranslated regions (UTRs) which may be involved in the translational control of the enzyme. In the present study we have used a series of stable transfectants of Chinese Hamster ovary cells expressing ODC mRNAs with various truncations in the 5′ and 3′ UTRs to investigate the importance of these regions. It is demonstrated that neither the 5′ UTR nor the 3′ UTR appears to be involved in the polyamine-mediated feedback control of ODC synthesis. The hypotonic induction of ODC, on the other hand, was shown to be highly dependent on the presence of the 3′ UTR, but not on the 5′ UTR, of ODC mRNA. Cells expressing ODC mRNAs lacking the 3′ UTR showed no, or only a very slight, induction of ODC whether the 5′ UTR was present or not, whereas the cell lines expressing ODC mRNAs containing the 3′ UTR (with or without the 5′ UTR) markedly induced ODC after a hypotonic shock. The present finding of a role for the ODC mRNA 3′ UTR in the hypotonic induction of ODC is the first demonstration of a specific effect of the 3′ UTR in the regulation of ODC.
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38

Waseem, Tatyana V., Sergei V. Konev, and Sergei V. Fedorovich. "Influence of Hypotonic Shock on Glutamate and GABA Uptake in Rat Brain Synaptosomes." Neurochemical Research 29, no. 9 (September 2004): 1653–58. http://dx.doi.org/10.1023/b:nere.0000035799.79422.d1.

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39

Fret, T., L. Heylen, M. Nuydens, F. De Jongh, and T. Meert. "Hypotonic shock in mice as in vivo model for cytotoxic brain oedema formation." European Journal of Anaesthesiology 25, Supplement 43 (January 2008): 1. http://dx.doi.org/10.1097/00003643-200801001-00001.

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40

Ubl, J., H. Murer, and H. A. Kolb. "Hypotonic shock evokes opening of Ca2+-activated K channels in opossum kidney cells." Pflügers Archiv - European Journal of Physiology 412, no. 5 (October 1988): 551–53. http://dx.doi.org/10.1007/bf00582547.

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41

Adorante, Joseph S., and Jeffrey L. Edelman. "Letters to the Editor." American Journal of Physiology-Cell Physiology 273, no. 4 (October 1, 1997): C1435—C1436. http://dx.doi.org/10.1152/ajpcell.1997.273.4.c1435.

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The following is the abstract of the article discussed in the subsequent letter: Mitchell, Claire H., Jin Jun Zhang, Liwei Wang, and Tim J. C. Jacob. Volume-sensitive chloride current in pigmented ciliary epithelial cells: role of phospholipases. Am. J. Physiol. 272 ( Cell Physiol. 41): C212–C222, 1997.—The whole cell recording technique was used to examine an outwardly rectifying chloride current activated by hypotonic shock in bovine pigmented ciliary epithelial (PCE) cells. Removal of internal and external Ca2+ did not affect the activation of these currents, but they were abolished by the phospholipase C inhibitor neomycin. The current was blocked by 5-nitro-2-(3-phenylpropylamino)benzoic acid, 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonic acid, and 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) in a voltage-dependent manner, but tamoxifen, dideoxyforskolin, and quinidine did not affect it. This blocking profile differs from that of the volume-sensitive chloride channel in neighboring nonpigmented ciliary epithelial cells (Wu, J., J. J. Zhang, H. Koppel, and T. J. C. Jacob. J. Physiol. Lond. 491: 743–755, 1996), and this difference implies that the volume responses of the two cell types are mediated by different chloride channels (Jacob, T. J. C., and J. J. Zhang. J. Physiol. Lond. In press). Intracellular administration of guanosine 5′- O-(3-thiotriphosphate) (GTPγS) to PCE cells induced a transient, time-independent, outwardly rectifying chloride current that closely resembled the current activated by hypotonic shock. DIDS produced a voltage-dependent block of the GTPγS-activated current similar to the block of the hypotonically activated current. Intracellular neomycin completely prevented activation of this current as did incubation of the cells in calphostin C, an inhibitor of protein kinase C (PKC). Removal of Ca2+ did not affect activation of the current by GTPγS but extended the duration of the response. Inhibition of phospholipase A2 (PLA2) with p-bromophenacyl bromide prevented the activation of the hypotonically induced current and also inhibited the current once activated by hypotonic solution. The findings imply that the hypotonic response in PCE cells is mediated by both phospholipase C (PLC) and PLA2. Both phospholipases generate arachidonic acid, and, in addition, the PLC pathway regulates the PLA2 pathway via a PKC-dependent phosphorylation of PLA2.
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42

Bianchini, L., B. Fossat, J. Porthe-Nibelle, and B. Lahlou. "Activation by N-ethylmaleimide of a Cl--dependent K+ flux in isolated trout hepatocytes." Journal of Experimental Biology 157, no. 1 (May 1, 1991): 335–48. http://dx.doi.org/10.1242/jeb.157.1.335.

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Isolated trout hepatocytes when swollen in hypotonic medium undergo a regulatory volume decrease (RVD), which occurs via KCl loss. The system shows characteristics similar to those of the transporter described in red cells. This led us to investigate, in trout hepatocytes, the effect of another signal known to activate this flux in red cells, i.e. treatment with the sulphhydryl-group reagent N-ethylmaleimide (NEM). NEM treatment resulted in a striking increase in ouabain-resistant K+ uptake measured by an isotope pulse uptake technique. The time course of the response to NEM was similar to that obtained with a hypotonic shock, indicating that the effect of NEM was immediate and transient. The NEM-stimulated K+ influx demonstrated the same anion sensitivity as the volume-induced K+ influx, i.e. a specific requirement for Br- or Cl-. Efflux experiments showed that NEM treatment produced a stimulation of both K+ and Cl- effluxes leading to a substantial net loss (10%) of cellular KCl, as confirmed by analysis of ionic contents. This KCl loss is consistent with the rapid cell shrinkage observed after addition of NEM. The Cl--dependent K+ influx was found to be independent of external Na+; in addition, NEM had no effect on Na+ content, indicating that Na+ is not implicated in this process. The effect of loop diuretics was tested on the NEM-stimulated K+ influx. As observed for the volume-induced K+ flux, a high concentration of furosemide (10(−3) mol l-1) is required for full inhibition of this flux; no effect was obtained with bumetanide (10(−4) mol l-1). Consequently, NEM appears to activate a KCl cotransport similar to the one induced in hypotonically swollen cells. Finally, the combination of the two treatments, NEM and hypotonic shock, was found to increase the K+ fluxes even further, suggesting additivity of the two stimuli by mutual positive interaction.
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43

Hoffmann, Tamara, Clara Boiangiu, Susanne Moses, and Erhard Bremer. "Responses of Bacillus subtilis to Hypotonic Challenges: Physiological Contributions of Mechanosensitive Channels to Cellular Survival." Applied and Environmental Microbiology 74, no. 8 (February 29, 2008): 2454–60. http://dx.doi.org/10.1128/aem.01573-07.

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ABSTRACT Mechanosensitive channels are thought to function as safety valves for the release of cytoplasmic solutes from cells that have to manage a rapid transition from high- to low-osmolarity environments. Subsequent to an osmotic down-shock of cells grown at high osmolarity, Bacillus subtilis rapidly releases the previously accumulated compatible solute glycine betaine in accordance with the degree of the osmotic downshift. Database searches suggest that B. subtilis possesses one copy of a gene for a mechanosensitive channel of large conductance (mscL) and three copies of genes encoding proteins that putatively form mechanosensitive channels of small conductance (yhdY, yfkC, and ykuT). Detailed mutational analysis of all potential channel-forming genes revealed that a quadruple mutant (mscL yhdY yfkC ykuT) has no growth disadvantage in high-osmolarity media in comparison to the wild type. Osmotic down-shock experiments demonstrated that the MscL channel is the principal solute release system of B. subtilis, and strains with a gene disruption in mscL exhibited a severe survival defect upon an osmotic down-shock. We also detected a minor contribution of the SigB-controlled putative MscS-type channel-forming protein YkuT to cellular survival in an mscL mutant. Taken together, our data revealed that mechanosensitive channels of both the MscL and MscS types play pivotal roles in managing the transition of B. subtilis from hyper- to hypo-osmotic environments.
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44

Nanduri, Jayasri, and Alan M. Tartakoff. "Perturbation of the Nucleus: A Novel Hog1p-independent, Pkc1p-dependent Consequence of Hypertonic Shock in Yeast." Molecular Biology of the Cell 12, no. 6 (June 2001): 1835–41. http://dx.doi.org/10.1091/mbc.12.6.1835.

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Hypertonic shock of Saccharomyces cerevisiaeactivates the Hog1p MAP kinase cascade. In contrast, protein kinase C (Pkc1p) and the “cell integrity” MAP kinase cascade are critical for the response to hypotonic shock. We observed that hypertonic shock transiently relocated many, but not all, nuclear and nucleolar proteins to the cytoplasm. We hypothesized that the relocation of nuclear proteins was due to activation of the Hog1p kinase cascade, yet, surprisingly, Hog1p was not required for these effects. In contrast, Pkc1p kinase activity was required, although the Pkc1p MAP kinase cascade and several factors known to lie upstream and downstream of Pkc1p were not. Moreover, sudden induction of a hyperactive form of Pkc1p was sufficient to relocate nuclear proteins. Taken together, these observations show that the scope of involvement of Pkc1p in the organization of the nucleus considerably exceeds what has been characterized previously. The relocation of nuclear proteins is likely to account for the profound inhibition of RNA synthesis that was observed during hypertonic shock.
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45

Solenov, Evgeny I. "Cell Volume and Sodium Content in Rat Kidney Collecting Duct Principal Cells During Hypotonic Shock." Journal of Biophysics 2008 (July 27, 2008): 1–5. http://dx.doi.org/10.1155/2008/420963.

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The purpose of this study was to investigate the time course of the volume-regulatory response and intracellular sodium concentration ([Na+]i) in the principal cells of rat kidney outer medulla collecting duct (OMCD) epithelia during acute swelling in hypotonic medium. Hypotonic shock was created by PBS diluted with 50% of water. Changes in cell volume were measured with calcein quenching method. Intracellular sodium concentration was studied with fluorescence dye Sodium Green. Principal cells of microdissected OMCD fragments swelled very fast. The characteristic time of swelling (τ1) was 0.65±0.05 seconds, and the volume increased more than 60% (92.9±5.6 and 151.3±9.8 μm3 control and peak volumes correspondently, P<.01). After cell volume reached the peak of swelling, the RVD began without lag period. The characteristic time of volume decreasing to new steady-state level (τ2) was 8.9±1.1 seconds. In hypoosmotic medium, cell volume stabilized on higher level in comparison with control (110.3±8.3 μm3, P<.01). After restoration of the medium osmolality to normotonic, cell volume stabilized on significantly low level in comparison with control level (71.4±6.1 μm3, P<.01). During the hypoosmotic shock, [Na+]i decreased from control level in isotonic PBS to the low level in hypoosmotic solution (27.7±1.4 and 5.8±0.23 mM, P<.01). Calculation of sodium content per cell has shown the significant sodium entry into the cells, which caused a temporary increase correlated with the peak of cell volume caused by swelling. The conclusion is made that in our model of hypoosmotic shock, swelling activates transporters with high permeability for Na+ that provides sodium flux into the cells.
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46

Avella, Martine, Olivier Ducoudret, Didier F. Pisani, and Philippe Poujeol. "Swelling-activated transport of taurine in cultured gill cells of sea bass: physiological adaptation and pavement cell plasticity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1149—R1160. http://dx.doi.org/10.1152/ajpregu.90615.2008.

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We have investigated volume-activated taurine transport and ultrastructural swelling response of sea bass gill cells in culture, assuming that euryhaline fish may have developed particularly efficient mechanisms of salinity adaptation. In vivo, when sea basses were progressively transferred from seawater to freshwater, we noticed a decrease in blood osmotic pressure. When gill cells in culture were subjected to 30% hypotonic shock, we observed a five-fold stimulation of [3H]taurine efflux. This transport was reduced by various anion channel inhibitors with the following efficiency: 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB) > niflumic acid > DIDS = diphenylamine-2-carboxylic acid. With polarized gill cells in culture, the hypotonic shock produced a five-fold stimulation of apical taurine transport, whereas basolateral exit was 25 times higher. Experiments using ionomycin, thapsigargin, BAPTA-AM, or removal of extracellular calcium suggested that taurine transport was regulated by external calcium. The inhibitory effects of lanthanum and streptomycin support Ca2+ entry through mechanosensitive Ca2+ channels. Branchial cells also showed hypotonically activated anionic currents sensitive to DIDS and NPPB. Similar pharmacology and time course suggested the potential existence of a common pathway for osmosensitive taurine and Cl− efflux through volume-sensitive organic osmolyte and anion channels. A three-dimensional structure study revealed that respiratory gill cells began to swell only 15 s after hypoosmotic shock. Apical microridges showed membrane outfoldings: the cell surface became smoother with a progressive disappearance of ridges. Therefore, osmotic swelling may not actually induce membrane stretch per se, inasmuch as the microridges may provide a reserve of surface area. This work demonstrates mechanisms of functional and morphological plasticity of branchial cells during osmotic stress.
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Meng, Qinglei, Zhenmin Bao, Zhaoping Wang, Shi Wang, Jingjie Hu, Xiaoli Hu, and Xiaoting Huang. "Growth and Reproductive Performance of Triploid Yesso Scallops (Patinopecten yessoensis) Induced by Hypotonic Shock." Journal of Shellfish Research 31, no. 4 (December 2012): 1113–22. http://dx.doi.org/10.2983/035.031.0422.

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48

Margenthaler, Julie A. "The potential role and mechanisms of distilled water-induced hypotonic shock on malignant cells." Journal of Surgical Research 181, no. 1 (May 2013): 67–68. http://dx.doi.org/10.1016/j.jss.2012.01.014.

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49

Ubl, Joachim, Heini Murer, and Hans Albert Kolb. "Simultaneous recording of cell volume, membrane current and membrane potential: effect of hypotonic shock." Pfl�gers Archiv European Journal of Physiology 415, no. 3 (December 1989): 381–83. http://dx.doi.org/10.1007/bf00370891.

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50

Jung, G., A. Dieterlen, E. Guerin, A. Brunot, J. Selva, and G. Schultz. "Size and Shape Change Behaviour of Platelets during Storage in Response to Hypotonic Shock." Vox Sanguinis 70, no. 1 (January 1996): 50–52. http://dx.doi.org/10.1111/j.1423-0410.1996.tb01001.x.

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