Amino Acid Correction of Regulatory Volume Decrease Evoked by Hypotonic Stress in Mouse Oocytes In Vitro

2015 ◽  
Vol 159 (1) ◽  
pp. 35-37 ◽  
Author(s):  
M. A. Pogorelova ◽  
V. A. Golichenkov ◽  
V. N. Pogorelova ◽  
A. I. Panait ◽  
A. A. Smirnov ◽  
...  
Keyword(s):  
Amino Acid ◽  
Regulatory Volume Decrease ◽  
Hypotonic Stress ◽  
Mouse Oocytes ◽  
Volume Decrease

scholarly journals Regulatory volume decrease in isolated nematocytes is affected by crude venom from the jellyfish Pelagia noctiluca

2014 ◽  
Vol 87 (2) ◽  
Author(s):  
Rossana Morabito ◽  
Silvia Dossena ◽  
Giuseppa La Spada ◽  
Angela Marino
Keyword(s):  
Cultured Cells ◽  
Cell Model ◽  
Regulatory Volume Decrease ◽  
Inhibitory Effect ◽  
Crude Venom ◽  
Trypan Blue Exclusion ◽  
Hypotonic Stress ◽  
Pelagia Noctiluca ◽  
Volume Decrease

Crude venom from nematocysts of the Scyphozoan <em>Pelagia noctiluca</em> possesses hemolytic and cytotoxic power on cultured cells and elicits local and systemic inflammation reactions <em>in vivo</em>. The ability of regulating their volume after exposure to an anisosmotic solution is a fundamental feature common to cells from vertebrates and invertebrates, including Cnidarians. The aim of the present work i s to assay whether crude venom from <em>Pelagia noctiluca</em> may affect the regulatory volume decrease (RVD) of nematocytes isolated from the Anthozoan <em>Aiptasia mutabilis</em>, here employed as a cell model. For this purpose, nematocytes were isolated by 605 mM NaSCN plus 0.01 mM Ca2+ application on acontia of <em>Aiptasia mutabilis</em>, while crude venom was obtained by sonication of a population of, respectively, 10, 25 and 50 nematocysts/µL (n/µL). Isolated nematocytes were pre-treated for 30 min with crude venom, submitted to hypotonic stress and their osmotic response and RVD were measured optically. Our results show that, after exposure to crude venom, nematocytes were morphologically intact, as shown by the Trypan blue exclusion test, but did not exhibit RVD. This effect was dose-dependent and reversed by the ionopho re gramicidin. The last observation suggests an inhibitory effect of venom on cell membrane ion transport mechanisms involved in RVD. Further studies are needed to verify this hypothesis and ascertain if a similar effect could be observed in human cells.

Cell volume increase and extracellular Ca2+ are needed for hyposmotically induced prolactin release in tilapia

2003 ◽  
Vol 284 (5) ◽  
pp. C1280-C1289 ◽  
Author(s):  
A. P. Seale ◽  
N. H. Richman ◽  
T. Hirano ◽  
I. Cooke ◽  
E. G. Grau
Keyword(s):  
Cell Volume ◽  
Regulatory Volume Decrease ◽  
Volume Increase ◽  
Solute Retention ◽  
Intracellular Ca ◽  
Freshwater Adaptation ◽  
Euryhaline Teleost ◽  
Volume Decrease

In the tilapia ( Oreochromis mossambicus), as in many euryhaline teleost fish, prolactin (PRL) plays a central role in freshwater adaptation, acting on osmoregulatory surfaces to reduce ion and water permeability and increase solute retention. Consistent with these actions, PRL release is stimulated as extracellular osmolality is reduced both in vivo and in vitro. In the current experiments, a perfusion system utilizing dispersed PRL cells was developed for permitting the simultaneous measurement of cell volume and PRL release. Intracellular Ca2+ was monitored using fura 2-loaded cells under the same conditions. When PRL cells were exposed to hyposmotic medium, an increase in PRL cell volume preceded the increase in PRL release. Cell volume increased in proportion to decreases of 15 and 30% in osmolality. However, regulatory volume decrease was clearly seen only after a 30% reduction. The hyposmotically induced PRL release was sharply reduced in Ca2+-deleted hyposmotic medium, although cell volume changes were identical to those observed in normal hyposmotic medium. In most cells, a rise in intracellular Ca2+ concentration ([Ca2+]i) during hyposmotic stimulation was dependent on the availability of extracellular Ca2+, although small transient increases in [Ca2+]i were sometimes observed upon introduction of Ca2+-deleted media of the same or reduced osmolality. These results indicate that an increase in cell size is a critical step in the transduction of an osmotic signal into PRL release and that the hyposmotically induced increase in PRL release is greatly dependent on extracellular Ca2+.

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.

Effect of osmotic swelling on K+ conductance in jejunal crypt epithelial cells

1992 ◽  
Vol 262 (6) ◽  
pp. G1021-G1026 ◽  
Author(s):  
R. J. MacLeod ◽  
P. Lembessis ◽  
J. R. Hamilton
Keyword(s):  
Epithelial Cells ◽  
Regulatory Volume Decrease ◽  
Channel Blockers ◽  
Osmotic Swelling ◽  
Hypotonic Stress ◽  
Cell Sizing ◽  
Hypotonic Swelling ◽  
Cl Conductance ◽  
Volume Decrease ◽  
Crypt Cells

To further elucidate differences in ion transport properties between jejunal crypt and villus cells, we compared the responses of purified cell suspensions to hypotonic stress using electronic cell sizing to evaluate volume changes and 86Rb and 36Cl efflux. After hypotonic swelling, villus enterocytes undergo a regulatory volume decrease (RVD) due to the loss of K+ and Cl- through volume-activated conductances. After 0.6x isotonic challenge in Na(+)-free medium, crypt cells exhibited only partial RVD, with t1/2 congruent to 15 min. The addition of a cation ionophore, gramicidin (0.25 microM), to hypotonically swollen crypt cells caused an accelerated RVD, which was complete with t1/2 congruent to 5 min. Crypt epithelial cells showed no volume-activated 86Rb efflux, but villus enterocytes had an increased rate of 86Rb efflux after hypotonic dilution (P less than 0.001). Gramicidin added to hypotonically diluted crypt cells greatly increased the rate of 86Rb efflux compared with controls. Both villus (30 s; P less than 0.005) and crypt (2 min; P less than 0.001) cells exhibited volume-activated 36Cl efflux in absence of gramicidin. Cl- channel blockers anthracene-9-carboxylate (9-AC, 300 microM) and indanyloxyacetic acid (IAA-94, 100 microM) prevented crypt RVD (P less than 0.001) in the presence of gramicidin. Ouabain (P less than 0.001) or K(+)-free Na(+)-containing medium, but not Ba2+ (5 mM) or quinine (100 microM), prevented crypt partial RVD. We conclude that crypt cells lack volume-activated K+ conductance. The RVD exhibited by crypt cells, although partial, was due to Cl- loss through a volume-activated Cl- conductance and Na+ loss via Na(+)-K(+)-ATPase.

Amino Acid Osmolytes in Regulatory Volume Decrease and Isovolumetric Regulation in Brain Cells: Contribution and Mechanisms

2000 ◽  
Vol 10 (5-6) ◽  
pp. 361-370 ◽  
Author(s):  
Herminia Pasantes-Morales ◽  
Rodrigo Franco ◽  
M. Eugenia Torres-Marquez ◽  
Karla Hernández-Fonseca ◽  
Arturo Ortega
Keyword(s):  
Amino Acid ◽  
Regulatory Volume Decrease ◽  
Brain Cells ◽  
Volume Decrease

Regulatory volume decrease stimulates bile flow, bile acid excretion, and exocytosis in isolated perfused rat liver

1992 ◽  
Vol 262 (5) ◽  
pp. G806-G812 ◽  
Author(s):  
R. Bruck ◽  
P. Haddad ◽  
J. Graf ◽  
J. L. Boyer
Keyword(s):  
Bile Acid ◽  
Bile Flow ◽  
Sodium Taurocholate ◽  
Regulatory Volume Decrease ◽  
Acid Excretion ◽  
K Channels ◽  
Hypotonic Stress ◽  
Bile Acid Excretion ◽  
Second Peak ◽  
Volume Decrease

To study the effect of volume regulation on bile secretory function, isolated perfused rat livers (IPRL) were exposed to hypotonic stress (45 mM NaCl) while bile flow and the biliary excretion of bile acids and horseradish peroxidase (HRP) were assessed. Hypotonic stress induced a biphasic increase in bile flow, which rose in the first minute from 1.1 +/- 0.2 to 1.7 +/- 0.1 microliter.min-1.g liver-1 (P less than 0.01), an effect attributed to rapid osmotic equilibration of water, then increased further between 3 and 5 min to 1.6 +/- 0.1 microliter.min-1.g liver-1 (P less than 0.01, followed by a subsequent return to baseline. HRP excretion in bile increased during the second peak of bile flow from 0.9 +/- 0.2 to 1.1 +/- 0.2 ng.min-1.g liver-1, P less than 0.01. Pretreatment with colchicine but not lumicolchicine completely abolished the latter increase in bile flow and HRP excretion as did BaCl2 (1 mM), an inhibitor of both K+ channels and regulatory volume decrease (RVD) in hepatocytes. When sodium taurocholate was infused (1 mumol/min), hypotonic stress induced an even larger increase in the second peak of bile flow (5.1 +/- 0.7 microliters/g liver, P less than 0.01) and higher rates of bile acid excretion than in control perfusions with bile acid (126.2 +/- 21.0 vs. 99.0 +/- 17.1 nmol.min-1.g liver-1, P less than 0.05). These data suggest that both bile flow and bile acid excretion are stimulated during RVD by mechanisms that involve both K+ channels and microtubule-dependent exocytosis at the canalicular (apical) membrane domain.

scholarly journals Volume-induced increase of anion permeability in human lymphocytes.

1982 ◽  
Vol 80 (6) ◽  
pp. 801-823 ◽  
Author(s):  
S Grinstein ◽  
C A Clarke ◽  
A Dupre ◽  
A Rothstein
Keyword(s):  
Mononuclear Cells ◽  
Human Lymphocytes ◽  
Regulatory Volume Decrease ◽  
Peripheral Blood Mononuclear ◽  
Hypotonic Stress ◽  
Anion Conductance ◽  
Direct Measurements ◽  
36Cl Fluxes ◽  
Relative Conductance ◽  
Volume Decrease

Peripheral blood mononuclear cells (PBM) readjust their volumes after swelling in hypotonic media. This regulatory volume decrease (RVD) is associated with a loss of cellular K+ and is thought to be promoted by an increased permeability to this ion. In contrast, no change in volume was observed when K+ permeability of PBM in isotonic media was increased to comparable or higher levels using valinomycin. Moreover, valinomycin-induced 86Rb+ loss in K+-free medium was considerably slower than in K+-rich medium. These results suggest that anion conductance limits net salt loss in isotonic media. Direct measurements of relative conductance confirmed that in volume-static cells, anion conductance is lower than that of K+. In volume-regulating cells depolarization occurred presumably as a result of increased anion conductance. Accordingly, the efflux of 36Cl from PBM was markedly increased by hypotonic stress. Since both membrane potential and intracellular 36Cl concentration are reduced in hypotonically swollen cells, the increased efflux is probably due to a change in Cl- permeability. Anions and cations seem to move independently through the volume-induced pathways: the initial rate of 86Rb uptake in swollen cells was not affected by replacement of external Cl- by SO=4; conversely, 36Cl fluxes were unaffected by substitution of K+ by Na+. The data indicate that anion conductance is rate-determining in salt and water loss from PBM. An increase in anion conductance is suggested to be the critical step of RVD of human PBM.

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