Regulatory volume increase in astrocytes exposed to hypertonic medium requires β1-adrenergic Na+/K+-ATPase stimulation and glycogenolysis

2014 ◽  
Vol 93 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Dan Song ◽  
Junnan Xu ◽  
Leif Hertz ◽  
Liang Peng
Keyword(s):  
Hypertonic Medium ◽  
Volume Increase ◽  
Regulatory Volume Increase

Na+/H+ exchange and osmotic shrinkage in isolated trout hepatocytes

1997 ◽  
Vol 200 (17) ◽  
pp. 2369-2376 ◽  
Author(s):  
B Fossat ◽  
J Porthé-Nibelle ◽  
S Pedersen ◽  
B Lahlou
Keyword(s):  
Rainbow Trout ◽  
Intracellular Ph ◽  
Extracellular Ph ◽  
Hypertonic Medium ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Hypertonic Stress ◽  
Amiloride Derivatives ◽  
Na Uptake ◽  
Rainbow Trout Liver

The ability of rainbow trout liver cells to regulate their intracellular pH (pHi) was studied using two methods on hepatocytes isolated by collagenase digestion: (i) by monitoring pHi with the fluorescent dye BCECF-AM, and (ii) by measuring the amiloride-sensitive uptake of 22Na, which represents Na+/H+ exchange. In low-Na+ medium (¾16mmoll-1), Na+ uptake was reduced by approximately 70% in the presence of amiloride derivatives (DMA or MPA, 10(-4)moll-1). Changing separately either the extracellular pH (pHe) or the intracellular pH (pHi, clamped by treating the cells with nigericin in the presence of 140mmoll-1 K+) between 6 and 8 induced an increase in the rate of Na+ uptake when pHe was raised or when pHi was reduced. When transferred to hypertonic medium, hepatocytes shrank to nearly 72% of their initial volume, and thereafter a slow and partial regulatory volume increase phase was observed, with an increase in the amiloride-sensitive rate of Na+ uptake and an increase in intracellular pH. As DIDS-sensitive Cl- uptake was concomitantly enhanced, it is suggested that hypertonic stress activates Na+/H+ and Cl-/HCO3- exchange.

Regulatory volume increase (RVI) and apoptotic volume decrease (AVD) in U937 cells in hypertonic medium

2011 ◽  
Vol 5 (5) ◽  
pp. 487-494 ◽  
Author(s):  
V. E. Yurinskaya ◽  
A. A. Rubashkin ◽  
A. V. Shirokova ◽  
A. A. Vereninov
Keyword(s):  
U937 Cells ◽  
Hypertonic Medium ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Apoptotic Volume Decrease ◽  
Volume Decrease

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.

Secondary regulatory volume increase conferred on Xenopus oocytes by expression of AE2 anion exchanger

1997 ◽  
Vol 272 (1) ◽  
pp. C191-C202 ◽  
Author(s):  
L. Jiang ◽  
M. N. Chernova ◽  
S. L. Alper
Keyword(s):  
Volume Regulation ◽  
Xenopus Oocytes ◽  
Disulfonic Acid ◽  
Functional Coupling ◽  
Intrinsic Volume ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Hypertonic Stimulation ◽  
Shrinkage Prior ◽  
Hypotonic Swelling

Xenopus oocytes lack volume regulation and Cl/anion-exchange (AE) activity but express endogenous Na+/H+ exchange (NHE). We postulated that expression in oocytes of heterologous anion exchangers might allow regulatory volume increase (RVI) via functional coupling with endogenous NHE. Expression of neither erythroid nor kidney isoforms of AE1 conferred any form of RVI. In contrast, although AE2 expression did not confer primary RVI, it did confer on oocytes secondary RVI, with a requirement for hypotonic swelling before hypertonic shrinkage. This secondary RVI required extracellular Cl- and Na+, was blocked by 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and amiloride, was bumetanide insensitive, and was blocked by prevention of intracellular alkalinization, all properties consistent with functional coupling of AE2-mediated Cl-/HCO3- exchange and endogenous NHE. RVI was unaffected by CO2-HCO3- or by partial oocyte Cl- depletion and was unrelated to the rate of oocyte shrinkage. Prior hypotonic swelling did not significantly alter subsequent hypertonic stimulation of AE2-mediated 36Cl influx or efflux. We conclude that heterologous AE2 expression suffices to confer volume regulation on Xenopus oocytes that lack intrinsic volume-regulatory mechanisms.

SRC family kinases in cell volume regulation

2005 ◽  
Vol 288 (3) ◽  
pp. C483-C493 ◽  
Author(s):  
David M. Cohen
Keyword(s):  
Tyrosine Kinases ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Src Family Kinases ◽  
Protein Tyrosine Kinases ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Hypotonic Stress ◽  
Cell Functions ◽  
Broad Role

SRC family kinases are a group of nine cytoplasmic protein tyrosine kinases essential for many cell functions. Some appear to be ubiquitously expressed, whereas others are highly tissue specific. The ability of members of the SRC family to influence ion transport has been recognized for several years. Mounting evidence suggests a broad role for SRC family kinases in the cell response to both hypertonic and hypotonic stress, and in the ensuing regulatory volume increase or decrease. In addition, members of this tyrosine kinase family participate in the mechanotransduction that accompanies cell membrane deformation. Finally, at least one SRC family member operates in concert with the p38 MAPK to regulate tonicity-dependent gene transcription.

Agonist-induced cytoplasmic volume changes in cultured rabbit parietal cells

2000 ◽  
Vol 279 (1) ◽  
pp. G40-G48 ◽  
Author(s):  
Thorsten Sonnentag ◽  
Wolf-Kristian Siegel ◽  
Oliver Bachmann ◽  
Heidi Rossmann ◽  
Andreas Mack ◽  
...  
Keyword(s):  
Volume Regulation ◽  
Parietal Cells ◽  
Cell Swelling ◽  
Secretory Process ◽  
Cell Shrinkage ◽  
Rapid Loss ◽  
Volume Changes ◽  
Volume Increase ◽  
Regulatory Volume Increase ◽  
Stimulation Of

Concomitant Na+/H+ and Cl−/HCO3 − exchange activation occurs during stimulation of acid secretion in cultured rabbit parietal cells, possibly related to a necessity for volume regulation during the secretory process. We investigated whether cytoplasmic volume changes occur during secretagogue stimulation of cultured rabbit parietal cells. Cells were loaded with the fluorescent dye calcein, and the calcein concentration within a defined cytoplasmic volume was recorded by confocal microscopy. Forskolin at 10−5 M, carbachol at 10−4 M, and hyperosmolarity (400 mosmol) resulted in a rapid increase in the cytoplasmic dye concentration by 21 ± 6, 9 ± 4, and 23 ± 5%, respectively, indicative of cell shrinkage, followed by recovery to baseline within several minutes, indicative of regulatory volume increase (RVI). Depolarization by 5 mM barium resulted in a decrease of the cytoplasmic dye concentration by 10 ± 2%, indicative of cell swelling, with recovery within 15 min, and completely prevented forskolin- or carbachol-induced cytoplasmic shrinkage. Na+/H+ exchange inhibitors slightly reduced the initial cell shrinkage and significantly slowed the RVI, whereas 100 μM bumetanide had no significant effect on either parameter. We conclude that acid secretagoguges induce a rapid loss of parietal cell cytoplasmic volume, followed by RVI, which is predominantly mediated by Na+/H+ and Cl−/HCO3 − exchange.

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.

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