scholarly journals Regulatory Volume Increase and Regulatory Volume Decrease Responses in HL-1 Atrial Myocytes

2014 ◽  
Vol 33 (6) ◽  
pp. 1745-1757 ◽  
Author(s):  
Veronica I. Cacace ◽  
Andres G. Finkelsteyn ◽  
Laura M. Tasso ◽  
Carlos F. Kusnier ◽  
Karina A. Gomez ◽  
...  
Keyword(s):  
Regulatory Volume Decrease ◽  
Atrial Myocytes ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Volume Decrease

Responses of lymphocytes to anisotonic media: volume-regulating behavior

1984 ◽  
Vol 246 (3) ◽  
pp. C204-C215 ◽  
Author(s):  
S. Grinstein ◽  
A. Rothstein ◽  
B. Sarkadi ◽  
E. W. Gelfand
Keyword(s):  
Regulatory Volume Decrease ◽  
Lymphocyte Subpopulations ◽  
Lymphoid Cells ◽  
Ionophore A23187 ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Cytoplasmic Acidification ◽  
Tissue Of Origin ◽  
Volume Decrease ◽  
Media Volume

The regulatory responses elicited in lymphoid cells suspended in anisotonic media are reviewed. The immediate response approximates osmometric behavior. In addition, in hypotonic media, the initial osmometric swelling is followed by a regulatory volume decrease (RVD), which is associated with KCl loss. The volume-induced effluxes of K+ and Cl- are mediated by two independent conductive pathways. Ca2+-depletion experiments and studies of inhibitor susceptibility suggest that Ca2+ may mediate the activation of the K+ pathway. The responses of the two main lymphocyte subpopulations to hypotonic challenge are different. RVD is much more rapid in T- than in B-cells, regardless of their tissue of origin. Under certain conditions, shrunken lymphocytes will regain their initial volume. This regulatory volume increase (RVI) is due to NaCl uptake, followed by a secondary exchange of Na+ for K+ via the Na+-K+ pump. Na+ is primarily taken up in exchange for H+ through an amiloride-sensitive pathway, whereas Cl- enters in exchange for HCO-3 (or OH-). Anion and cation fluxes responsible for RVI are electroneutral. Some of the volume-sensitive pathways can also be activated in isotonic cells. The conductive K+ pathway is activated by Ca2+ plus ionophore A23187, and the Na+-H+ exchanger can be activated by cytoplasmic acidification. The responses of lymphocytes to anisotonic challenge are compared with those of other cells, and the possible significance of the volume-induced fluxes is discussed.

Ion transport asymmetry and functional coupling in bovine pigmented and nonpigmented ciliary epithelial cells

1994 ◽  
Vol 266 (5) ◽  
pp. C1210-C1221 ◽  
Author(s):  
J. L. Edelman ◽  
G. Sachs ◽  
J. S. Adorante
Keyword(s):  
Transport Properties ◽  
Aqueous Humor ◽  
Lucifer Yellow ◽  
Regulatory Volume Decrease ◽  
Ciliary Epithelium ◽  
Functional Coupling ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Cell Sizing ◽  
Volume Decrease

The solute and water transport properties of the bovine ciliary epithelium were studied using isolated pigmented (PE) and nonpigmented (NPE) cells. It was shown that these cells were functionally coupled by demonstrating dye diffusion between paired PE and NPE cells after microinjection of lucifer yellow. Electronic cell sizing was used to measure cell volume changes of isolated PE and NPE cells in suspension after anisosmotic perturbations and after transport inhibition under isosmotic conditions. The PE cells showed the presence of a regulatory volume increase when subjected to osmotic shrinkage with NaCl, whereas the NPE cells did not demonstrate a regulatory volume increase under these conditions. In contrast, the NPE cells exhibited a regulatory volume decrease when subjected to osmotic swelling, whereas the PE cells did not recover from swelling. The regulatory volume decrease in NPE cells was inhibited by increased bath K or pretreatment with quinine (1 mM). The presence of a bumetanide-sensitive mechanism capable of moving measurable amounts of solute and water, probably Na-K-2Cl cotransport, was demonstrated in the PE cells but absent in the NPE cells. Bumetanide produced a dose-dependent shrinkage of PE cells at concentrations as low as 1 microM. Isosmotically reducing bath Cl, Na, or K concentration caused a rapid shrinkage of PE cells that was bumetanide inhibitable. The asymmetry of transport properties in PE and NPE cells supports a functional syncytium model of aqueous humor formation (39) across the two layers of the ciliary epithelium wherein ion uptake from the blood is carried out by the PE cells and ion extrusion by the NPE cells. Gap-junction coupling between the cells allows the ions taken up by the PE cells to move into the NPE cells. Extrusion of Na by the Na-K pump across the aqueous facing (basolateral) membranes of the NPE cells, most likely accompanied by Cl, determines the formation of the aqueous humor.

scholarly journals Vasopressin Neurons Respond to Hyperosmotic Stimulation with Regulatory Volume Increase and Secretory Volume Decrease by Activating Ion Transporters and Ca2+ Channels

2021 ◽  
Vol 55 (S1) ◽  
pp. 119-134
Keyword(s):  
Regulatory Volume Decrease ◽  
The Body ◽  
Cell Swelling ◽  
Ion Transporters ◽  
Cell Shrinkage ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Vasopressin Neurons ◽  
Ca2 Channels ◽  
Volume Decrease

BACKGROUND/AIMS: Arginine vasopressin (AVP) neurons play an important role for sensing a change in the plasma osmolarity and thereby responding with regulated AVP secretion in order to maintain the body fluid homeostasis. The osmo-sensing processes in magnocellular neurosecretory cells (MNCs) including AVP and oxytocin (OXT) neurons of the hypothalamus were reported to be coupled to sustained osmotic shrinkage or swelling without exhibiting discernible cell volume regulation. Since increasing evidence has shown some important differences in properties between AVP and OXT neurons, osmotic volume responses are to be reexamined with distinguishing these cell types from each other. We previously reported that AVP neurons identified by transgenic expression of enhanced green fluorescence protein (eGFP) possess the ability of regulatory volume decrease (RVD) after hypoosmotic cell swelling. Thus, in the present study, we examined the ability of regulatory volume increase (RVI) after hyperosmotic cell shrinkage in AVP neurons. METHODS: Here, we used eGFP-identified AVP neurons acutely dissociated from AVP-eGFP transgenic rats. We performed single-cell size measurements, cytosolic RT-PCR analysis, AVP secretion measurements, and patch-clamp studies. RESULTS: The AVP neurons were found to respond to a hyperosmotic challenge with physiological cell shrinkage caused by massive secretion of AVP, called a secretory volume decrease (SVD), superimposed onto physical osmotic cell shrinkage, and also to exhibit the ability of RVI coping with osmotic and secretory cell shrinkage. Furthermore, our pharmacological and molecular examinations indicated that AVP secretion and its associated SVD event are triggered by activation of T-type Ca2+ channels, and the RVI event is attained by parallel operation of Na+/H+ exchanger and Cl-/HCO3- anion exchanger. CONCLUSION: Thus, it is concluded that AVP neurons respond to hyperosmotic stimulation with the regulatory volume increase and the secretory volume increase by activating ion transporters and Ca2+ channels, respectively.

Volume-Regulatory Ion Channels in Epithelial Cells

Physiology ◽  
1989 ◽  
Vol 4 (6) ◽  
pp. 238-242 ◽  
Author(s):  
Y Okada ◽  
A Hazama
Keyword(s):  
Ion Channels ◽  
Epithelial Cells ◽  
Patch Clamp ◽  
Intestinal Epithelial Cells ◽  
Regulatory Volume Decrease ◽  
Intestinal Epithelial ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Whole Cell Recordings ◽  
Volume Decrease

Patch-clamp studies showed that the regulatory volume decrease process is closely associated with functions of K+, Cl-, and Ca2+-permeable channels in epithelial cells. Na+-permeable channels in the regulatory volume increase process may also be involved, as deduced from whole cell recordings using intestinal epithelial cells.

scholarly journals Hypertonic stress increases the Na+ conductance of rat hepatocytes in primary culture.

1995 ◽  
Vol 105 (4) ◽  
pp. 507-535 ◽  
Author(s):  
F Wehner ◽  
H Sauer ◽  
R K Kinne
Keyword(s):  
Cell Membrane ◽  
Primary Culture ◽  
Regulatory Volume Decrease ◽  
Rat Hepatocytes ◽  
Laser Scanning Microscopy ◽  
Specific Cell ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Hypertonic Stress ◽  
Cell Volumes

We studied the ionic mechanisms underlying the regulatory volume increase of rat hepatocytes in primary culture by use of confocal laser scanning microscopy, conventional and ion-sensitive microelectrodes, cable analysis, microfluorometry, and measurements of 86Rb+ uptake. Increasing osmolarity from 300 to 400 mosm/liter by addition of sucrose decreased cell volumes to 88.6% within 1 min; thereafter, cell volumes increased to 94.1% of control within 10 min, equivalent to a regulatory volume increase (RVI) by 44.5%. This RVI was paralleled by a decrease in cell input resistance and in specific cell membrane resistance to 88 and 60%, respectively. Ion substitution experiments (high K+, low Na+, low Cl-) revealed that these membrane effects are due to an increase in hepatocyte Na+ conductance. During RVI, ouabain-sensitive 86Rb+ uptake was augmented to 141% of control, and cell Na+ and cell K+ increased to 148 and 180%, respectively. The RVI, the increases in Na+ conductance and cell Na+, as well as the activation of Na+/K(+)-ATPase were completely blocked by 10(-5) mol/liter amiloride. At this concentration, amiloride had no effect on osmotically induced cell alkalinization via Na+/H+ exchange. When osmolarity was increased from 220 to 300 mosm/liter (by readdition of sucrose after a preperiod of 15 min in which the cells underwent a regulatory volume decrease, RVD) cell volumes initially decreased to 81.5%; thereafter cell volumes increased to 90.8% of control. This post-RVD-RVI of 55.0% is also mediated by an increase in Na+ conductance. We conclude that rat hepatocytes in confluent primary culture are capable of RVI as well as of post-RVD-RVI. In this system, hypertonic stress leads to a considerable increase in cell membrane Na+ conductance. In concert with conductive Na+ influx, cell K+ is then increased via activation of Na+/K(+)-ATPase. An additional role of Na+/H+ exchange in the volume regulation of rat hepatocytes remains to be defined.

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+.

Does the intracellular ionic concentration or the cell water content (cell volume) determine the activity of TonEBP in NIH3T3 cells?

2008 ◽  
Vol 295 (6) ◽  
pp. C1528-C1534 ◽  
Author(s):  
Tina Rødgaard ◽  
Kenneth Schou ◽  
Martin B. Friis ◽  
Else K. Hoffmann
Keyword(s):  
Regulatory Volume Decrease ◽  
Ionic Concentration ◽  
Luciferase Assay ◽  
Cell Shrinkage ◽  
Nih3t3 Cells ◽  
Hypertonic Medium ◽  
Volume Increase ◽  
Expression Of Genes ◽  
Enhancer Binding Protein ◽  
Volume Decrease

The transcription factor, tonicity-responsive enhancer binding protein (TonEBP), is involved in the adaptive response against hypertonicity. TonEBP regulates the expression of genes that catalyze the accumulation of osmolytes, and its transcriptional activity is increased by hypertonicity. The goal of the present investigation was to investigate whether cell shrinkage or high intracellular ionic concentration induced the activation of TonEBP. We designed a model system for isotonically shrinking cells over a prolonged period of time. Cells swelled in hypotonic medium and performed a regulatory volume decrease. Upon return to the original isotonic medium, cells shrank initially, followed by a regulatory volume increase. To maintain cell shrinkage, the RVI process was inhibited as follows: ethyl-isopropyl-amiloride inhibited the Na+/H+ antiport, bumetanide inhibited the Na+-K+-2Cl− cotransporter, and gadolinium inhibited shrinkage-activated Na+ channels. Cells remained shrunken for at least 4 h (isotonically shrunken cells). The activity of TonEBP was investigated with a Luciferase assay after isotonic shrinkage and after shrinkage in a high-NaCl hypertonic medium. We found that TonEBP was strongly activated after 4 and 16 h in cells in high-NaCl hypertonic medium, but not after 4 or 16 h in isotonically shrunken cells. Cells treated with high-NaCl hypertonic medium for 4 h had significantly higher intracellular concentrations of both K+ and Na+ than isotonically shrunken cells. This strongly suggested that an increase in intracellular ionic concentration and not cell shrinkage is involved in TonEBP activation.

Effects of arginine vasopressin on cell volume regulation in brain astrocyte in culture

1999 ◽  
Vol 276 (3) ◽  
pp. E596-E601 ◽  
Author(s):  
Darya Sarfaraz ◽  
Cosmo L. Fraser
Keyword(s):  
Cell Volume ◽  
Arginine Vasopressin ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Hypotonic Medium ◽  
Receptor Antagonists ◽  
Volume Increase ◽  
Glucose Water ◽  
Water Space ◽  
Volume Decrease

Astrocytes initially swell when exposed to hypotonic medium but rapidly return to normal volume by the process of regulatory volume decrease (RVD). The role that arginine vasopressin (AVP) plays in hypotonically mediated RVD in astrocytes is unknown. This study was therefore designed to determine whether AVP might play a role in astrocyte RVD. With the use of 3- O-[3H]methyl-d-glucose to determine water space, AVP treatment resulted in significantly increased 3- O-methyl-d-glucose water space within 30 s of hypotonic exposure ( P = 0.0001) and remained significantly elevated above baseline (1.75 μl/mg protein) at 5 min ( P < 0.021). In contrast, in untreated cells, complete RVD was achieved by 5 min. At 30 s, cell volume with AVP treatment was 37% greater than in cells that received no treatment (2.9 vs. 2.26 μl/mg protein, respectively; P < 0.006). The rate of cell volume increase (dV/d t) over 30 s was highly significant (0.038 vs. 0.019 μl ⋅ mg protein−1 ⋅ s−1in the AVP-treated vs. untreated group; P = 0.0004 by regression analysis). Additionally, the rate of cell volume decrease over the next 4.5 min was also significantly greater with vasopressin treatment (−dV/d t = 0.0027 vs. 0.0013 μl ⋅ mg protein−1 ⋅ s−1; P = 0.0306). The effect of AVP was concentration dependent with EC50= 3.5 nM. To determine whether AVP action was receptor mediated, we performed RVD studies in the presence of the V1-receptor antagonists benzamil and ethylisopropryl amiloride and the V2-receptor agonist 1-desamino-8-d-arginine vasopressin (DDAVP). Both V1-receptor antagonists significantly inhibited AVP-mediated volume increase by 40–47% ( P < 0.005), whereas DDAVP had no stimulatory effects above control. Taken together, these data suggest that AVP treatment of brain astrocytes in culture appears to increase 3- O-methyl-d-glucose water space during RVD through V1receptor-mediated mechanisms. The significance of these findings is presently unclear.

scholarly journals Dual Response of Human Leukemia U937 Cells to Hypertonic Shrinkage: Initial Regulatory Volume Increase (RVI) and Delayed Apoptotic Volume Decrease (AVD)

2012 ◽  
Vol 30 (4) ◽  
pp. 964-973 ◽  
Author(s):  
Valentina E. Yurinskaya ◽  
Alexey V. Moshkov ◽  
Anna V. Wibberley ◽  
Florian Lang ◽  
Michael A. Model ◽  
...  
Keyword(s):  
Human Leukemia ◽  
U937 Cells ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Apoptotic Volume Decrease ◽  
Dual Response ◽  
Volume Decrease
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