Regulatory volume increase after hypertonicity- or vasoactive-intestinal-peptide-induced cell-volume decrease in small-intestinal crypts is dependent on Na+-K+-2Cl? cotransport

1993 ◽  
Vol 423-423 (1-2) ◽  
pp. 67-73 ◽  
Author(s):  
J. A. O'Brien ◽  
R. J. Walters ◽  
M. A. Valverde ◽  
F. V. Sep�lveda
Keyword(s):  
Cell Volume ◽  
Vasoactive Intestinal Peptide ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Small Intestinal ◽  
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.

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+.

Proximal tubule volume regulation in hyperosmotic media: intracellular K+, Na+, and Cl-

1989 ◽  
Vol 257 (6) ◽  
pp. C1093-C1100 ◽  
Author(s):  
L. Rome ◽  
J. Grantham ◽  
V. Savin ◽  
J. Lohr ◽  
C. Lechene
Keyword(s):  
Proximal Tubule ◽  
Cell Volume ◽  
Volume Regulation ◽  
Electron Probe ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Cell Shrinkage ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Expected Increase

Nonperfused proximal S2 segments from rabbit kidney cortex have been shown to keep cell volume constant as medium osmolality is slowly raised but to shrink and not exhibit regulatory volume increase (RVI) if medium osmolality is abruptly elevated (J. Lohr and J. Grantham. J. Clin. Invest. 78: 1165-1172, 1986). In the current study, 0.5 mM butyrate in the medium 1) extended the range from 361 to 450 mosmol/kgH2O over which cells maintained volume constant as osmolality was gradually raised and 2) restored RVI after cell shrinkage when osmolality was rapidly raised from 295 to 400 mosmol/kgH2O. Volume regulation was associated with net increases in intracellular Na+ and Cl- but no change in K+ (measured by electron probe). The increments in Na+ and Cl- were insufficient to account for the total addition of osmolytes required for volume maintenance or restoration. The fraction of the expected increase in intracellular osmoles accounted for by the increase in [(K+)i + (Na+)i + (Cl-)i] was 52 and 21% for gradual and rapid osmotic changes, respectively. We conclude that butyrate enhances the capacity of S2 segments to regulate volume in hyperosmotic medium by promoting addition of Na+ and Cl- and by other undermined factors.

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

Mechanisms of secretion-associated shrinkage and volume recovery in cultured rabbit parietal cells

2007 ◽  
Vol 292 (3) ◽  
pp. G711-G717 ◽  
Author(s):  
Oliver Bachmann ◽  
Alexander Heinzmann ◽  
Andreas Mack ◽  
Michael P. Manns ◽  
Ursula Seidler
Keyword(s):  
Acid Secretion ◽  
Cell Volume ◽  
Parietal Cells ◽  
Cell Shrinkage ◽  
Volume Changes ◽  
Volume Increase ◽  
Initial Cell ◽  
Water Secretion ◽  
Dimethyl Amiloride ◽  
Volume Decrease

We have previously shown that stimulation of acid secretion in parietal cells causes rapid initial cell shrinkage, followed by Na+/H+ exchange-mediated regulatory volume increase (RVI). The factors leading to the initial cell shrinkage are unknown. We therefore monitored volume changes in cultured rabbit parietal cells by confocal measurement of the cytoplasmic calcein concentration. Although blocking the presumably apically located K+ channel KCNQ1 with chromanol 293b reduced both the forskolin- and carbachol-induced cell shrinkage, inhibition of Ca2+-sensitive K+ channels with charybdotoxin strongly inhibited the cell volume decrease after carbachol, but not after forskolin stimulation. The cell shrinkage induced by both secretagogues was partially inhibited by blocking H+-K+-ATPase with SCH28080 and completely absent after incubation with NPPB, which inhibits parietal cell anion conductances involved in acid secretion. The subsequent RVI was strongly inhibited with the Na+/H+ exchanger 1 (NHE1)-specific concentration of HOE642 and completely by 500 μM dimethyl-amiloride (DMA), which also inhibits NHE4. None of the above substances induced volume changes under baseline conditions. Our results indicate that cell volume decrease associated with acid secretion is dependent on the activation of K+ and Cl− channels by the respective secretagogues. K+, Cl−, and water secretion into the secretory canaliculi is thus one likely mechanism of stimulation-associated cell shrinkage in cultured parietal cells. The observed RVI is predominantly mediated by NHE1.

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.

Cell volume control in vestibular dark cells during and after a hyposmotic challenge

1994 ◽  
Vol 266 (4) ◽  
pp. C1046-C1060 ◽  
Author(s):  
P. Wangemann ◽  
N. Shiga
Keyword(s):  
Cell Volume ◽  
Volume Control ◽  
Cell Width ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Dark Cells ◽  
Cell Height ◽  
Vestibular Dark Cells ◽  
Cell Volume Control

Cell height was measured as an index of volume in a preparation of vestibular dark cells in which the perfusate had access to both sides of the epithelium. In response to a hyposmotic challenge induced by removal of 75 mM NaCl, cell height increased to 107%; however, cell width did not increase. Significantly larger increases in cell height were observed in the absence of Cl- or K+ or in the presence of ouabain, lidocaine, barium, or quinidine, at 7 degrees C, or after fixation with glutaraldehyde. However, no significantly different swelling was observed during a hyposmotic challenge in the absence of Na+ or in the presence of bumetanide or ethoxyzolamide. Subsequent return to control osmolarity caused a regulatory volume increase that was dependent on Na+, Cl-, and K+, inhibited by bumetanide, ouabain, or 7 degrees C, however not inhibited by ethoxyzolamide, barium, quinidine, or lidocaine. The data suggest that cell volume control during the hyposmotic challenge involved a mechanism dependent on cytosolic KCl and the Na(+)-K(+)-ATPase and that the Na(+)-Cl(-)-K+ cotransporter was involved in regulatory volume increase.

Astrocytes from Na+-K+-Cl−cotransporter-null mice exhibit absence of swelling and decrease in EAA release

2002 ◽  
Vol 282 (5) ◽  
pp. C1147-C1160 ◽  
Author(s):  
Gui Su ◽  
Douglas B. Kintner ◽  
Michael Flagella ◽  
Gary E. Shull ◽  
Dandan Sun
Keyword(s):  
Cell Volume ◽  
Glutamate Release ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
A Value ◽  
Cortical Astrocytes ◽  
High K ◽  
Stimulation Of

We reported previously that inhibition of Na+-K+-Cl− cotransporter isoform 1 (NKCC1) by bumetanide abolishes high extracellular K+concentration ([K+]o)-induced swelling and intracellular Cl− accumulation in rat cortical astrocytes. In this report, we extended our study by using cortical astrocytes from NKCC1-deficient (NKCC1−/−) mice. NKCC1 protein and activity were absent in NKCC1−/− astrocytes. [K+]o of 75 mM increased NKCC1 activity approximately fourfold in NKCC1+/+ cells ( P< 0.05) but had no effect in NKCC1−/− astrocytes. Intracellular Cl− was increased by 70% in NKCC1+/+ astrocytes under 75 mM [K+]o ( P < 0.05) but remained unchanged in NKCC1−/− astrocytes. Baseline intracellular Na+ concentration ([Na+]i) in NKCC1+/+ astrocytes was 19.0 ± 0.5 mM, compared with 16.9 ± 0.3 mM [Na+]i in NKCC1−/− astrocytes ( P < 0.05). Relative cell volume of NKCC1+/+ astrocytes increased by 13 ± 2% in 75 mM [K+]o, compared with a value of 1.0 ± 0.5% in NKCC1−/− astrocytes ( P < 0.05). Regulatory volume increase after hypertonic shrinkage was completely impaired in NKCC1−/− astrocytes. High-[K+]o-induced 14C-labeledd-aspartate release was reduced by ∼30% in NKCC1−/− astrocytes. Our study suggests that stimulation of NKCC1 is required for high-[K+]o-induced swelling, which contributes to glutamate release from astrocytes under high [K+]o.

Sign in / Sign up

Export Citation Format

Share Document