scholarly journals Volume-activated chloride permeability can mediate cell volume regulation in a mathematical model of a tight epithelium.

1990 ◽  
Vol 96 (2) ◽  
pp. 319-344 ◽  
Author(s):  
J Strieter ◽  
J L Stephenson ◽  
L G Palmer ◽  
A M Weinstein
Keyword(s):  
Mathematical Model ◽  
Cell Volume ◽  
Volume Regulation ◽  
Electrical Potential ◽  
Cell Volume Regulation ◽  
York Academy ◽  
Constant Field ◽  
Chloride Permeability ◽  
Volume Regulatory Decrease ◽  
Tight Epithelium

Cell volume regulation during anisotonic challenge is investigated in a mathematical model of a tight epithelium. The epithelium is represented as compliant cellular and paracellular compartments bounded by mucosal and serosal bathing media. Model variables include the concentrations of Na, K, and Cl, hydrostatic pressure, and electrical potential, and the mass conservation equations have been formulated for both steady-state and time-dependent problems. Ionic conductance is represented by the Goldman constant field equation (Civan, M.M., and R.J. Bookman. 1982. Journal of Membrane Biology. 65:63-80). A basolateral cotransporter of Na, K, and Cl with 1:1:2 stoichiometry (Geck, P., and E. Heinz. 1980. Annals of the New York Academy of Sciences. 341:57-62.) and volume-activated basolateral ion permeabilities are incorporated in the model. MacRobbie and Ussing (1961. Acta Physiologica Scandinavica. 53:348-365.) reported that the cells of frog skin exhibit osmotic swelling followed by a volume regulatory decrease (VRD) when the serosal bath is diluted to half the initial osmolality. Similar regulation is achieved in the model epithelium when both a basolateral cotransporter and a volume-activated Cl permeation path are included. The observed transepithelial potential changes could only be simulated by allowing volume activation of the basolateral K permeation path. The fractional VRD, or shrinkage as percent of initial swelling, is examined as a function of the hypotonic challenge. The fractional VRD increases with increasing osmotic challenge, but eventually declines under the most severe circumstances. This analysis demonstrates that the VRD response depends on the presence of adequate intracellular chloride stores and the volume sensitivity of the chloride channel.

scholarly journals Proximal tubule volume regulation in hypo-osmotic media: intracellular K+, Na+, and Cl-.

1990 ◽  
Vol 1 (2) ◽  
pp. 211-218
Author(s):  
L Rome ◽  
C Lechene ◽  
J J Grantham
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Volume Regulatory Decrease ◽  
Osmotic Change ◽  
Electrolyte Loss ◽  
The Difference

This study sought to measure the net loss of intracellular K+, Na+, and Cl- that accompanied isosmotic cell volume regulation in hypotonic media and to determine if electrolyte loss depended on the rate at which the extracellular osmolality was reduced. Isolated nonperfused proximal S2 segments from rabbit kidney cortex were studied in vitro. Gradual lowering of osmolality from 295 to 150 mOsm/kg at a rate of 2 mOsm/kg/min did not cause an increase in tubule cell volume until the medium osmolality decreased below 190 mOsm/kg. By contrast, tubules rapidly bathed in low osmolality media exhibited classical osmometric swelling followed by incomplete volume regulatory decrease. Volume regulation associated with gradual and rapid lowering of osmolality was accompanied by the net loss of intracellular K+, Na+, and Cl- (measured by electron probe); however, the temporal pattern of electrolyte loss depended on the rate of osmotic change. With gradual lowering of osmolality, cell K+ content did not decrease significantly until osmolality was lowered below 200 mOsm/kg, whereas Cl- was lost at the 200 mOsm/kg level and below. With rapid lowering of osmolality, cell K+ content was strikingly decreased at the 200 mOsm/kg level, but Cl- did not change appreciably until osmolality was decreased to 150 mOsm/kg. Cell Na+ content decreased in hypo-osmotic media, but the magnitude was relatively small. During volume regulation that accompanied either gradual or rapid lowering of medium osmolality from 295 to 150 mOsm/kg, intracellular osmolal gap, the difference between medium osmolality and the sum of intracellular concentrations of K+, Na+, and Cl- decreased 87 and 58 mOsm/kg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

A mathematical model of the cell volume regulation in a hypotonic medium

2011 ◽  
Vol 437 (1) ◽  
pp. 79-81 ◽  
Author(s):  
E. I. Solenov ◽  
A. V. Ilyaskin ◽  
G. S. Baturina ◽  
D. A. Medvedev ◽  
A. P. Ershov ◽  
...  
Keyword(s):  
Mathematical Model ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Hypotonic Medium

scholarly journals Mathematical Model of Lacrimal Acinar Cell Volume Regulation and Solute Transport

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Wei Chieh Huang ◽  
Chris Clause ◽  
Peter Brink ◽  
Benjamin Walcott ◽  
Leon C Moore
Keyword(s):  
Mathematical Model ◽  
Solute Transport ◽  
Cell Volume ◽  
Acinar Cell ◽  
Volume Regulation ◽  
Cell Volume Regulation

Cell volume regulation in rat thin ascending limb of Henle's loop

1992 ◽  
Vol 263 (3) ◽  
pp. F353-F362
Author(s):  
L. F. Onuchic ◽  
I. R. Arenstein ◽  
A. G. Lopes
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Osmotic Shock ◽  
Basolateral Membrane ◽  
Cell Volume Regulation ◽  
Tetraacetic Acid ◽  
Volume Regulatory Decrease ◽  
Henle's Loop ◽  
Volume Regulatory Increase

Thin ascending limb cells of Henle's loop from Wistar rats were studied with in vitro microperfusion and video-optical techniques to investigate their ability in regulating cell volume during osmotic shock and to identify mechanisms of ion transport involved in the process. These cells showed a clear volume regulatory decrease (VRD) response in hyposmotic medium, but no volume regulatory increase in hyperosmotic medium. The presence of barium in the bath abolished VRD. Removal of K+ from bath and perfusate also inhibited the VRD response. Reintroduction of K+ in hyposmotic conditions reestablished cell volume regulation. Introduction of anthracene-9-COOH to the basolateral medium blocked cell volume regulatory response. Cl- removal from perfusate and bath solutions also inhibited VRD, probably because of a significant intracellular Cl- depletion. Exposure of cells to ethylene glycol-bis(beta-aminoethyl ether)-N,N,N'N'-tetraacetic acid in perfusate and bath solutions reduced significantly Ca2+ concentration and impaired VRD. Reintroduction of Ca2+ in hyposmotic conditions restored volume regulation. The presence of ouabain in basolateral medium also inhibited VRD. These data suggest that the following mechanisms in the basolateral membrane are involved in VRD response: K+ and Cl- conductive pathways, which might be Ca2+ dependent for activation, and an Na(+)-K(+)-adenosinetriphosphatase.

scholarly journals Mathematical model of interactions between cell volume regulation and transport in cortical TAL cells

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Aniel Nieves‐Gonzalez ◽  
Chris Clausen ◽  
Harold E Layton ◽  
Leon C Moore
Keyword(s):  
Mathematical Model ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation

Model of renal cell volume regulation without active transport: role of a heteroporous membrane

1988 ◽  
Vol 255 (3) ◽  
pp. F529-F538
Author(s):  
D. J. Welling ◽  
L. W. Welling
Keyword(s):  
Hydrostatic Pressure ◽  
Cell Volume ◽  
Active Transport ◽  
Volume Regulation ◽  
Essential Feature ◽  
Cell Volume Regulation ◽  
Reflection Coefficients ◽  
Renal Tubules ◽  
Volume Regulatory Decrease ◽  
Metabolic Substrates

Isolated proximal renal tubules of rabbit reach a passive steady-state volume in isotonic medium after active transport is inhibited by ouabain or by inhibition of cellular metabolism or lack of metabolic substrates. If the tubules are then placed in a hypotonic NaCl medium they swell rapidly and then exhibit a volume regulatory decrease (VRD) similar to that seen when active transport is present. We have mathematically modeled these transient events by assuming that the basolateral cell membrane is permeated by pores having at least two distinct reflection coefficients with respect to sodium, potassium, and chloride. VRD depends on the difference of the values of the reflection coefficients of the pore types. As hydrostatic pressure is exerted by the stretching basement membrane, water and ions can be expelled from the cells across the lower reflection coefficient pores and cause VRD. When the hydrostatic pressure compliance is removed, the cells fail to volume decrease unless sufficient extracellular impermeant solute is present to provide an osmotic force for water and ion exit. We conclude that a heteroporous membrane may be an essential feature for cell volume regulation and maintenance.

Basolateral membrane chloride permeability of A6 cells: implication in cell volume regulation

1995 ◽  
Vol 431 (1) ◽  
pp. 32-45 ◽  
Author(s):  
E. Brochiero ◽  
U. Banderali ◽  
S. Lindenthal ◽  
C. Raschi ◽  
J. Ehrenfeld
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Basolateral Membrane ◽  
Cell Volume Regulation ◽  
Chloride Permeability ◽  
A6 Cells
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