scholarly journals The Response of Duck Erythrocytes to Hypertonic Media

1971 ◽  
Vol 58 (4) ◽  
pp. 396-412 ◽  
Author(s):  
Floyd M. Kregenow

The addition of a hypertonic bathing medium to duck erythrocytes results in an initial instantaneous phase of osmotic shrinkage and, when the [K]o of the hypertonic solution is larger than "normal," in a second, more prolonged phase, the volume regulatory phase. During the latter, which also requires extracellular Na, the cells swell until they approach their initial isotonic volume. The increase in cell volume during the volume regulatory phase is accomplished by a gain in the cell content of K, Cl, and H2O. There is also a smaller increase in the Na content of the cell. Potassium is accumulated against an electrochemical gradient and is therefore actively transported into the cell. This accumulation is associated with an increase, although dissimilar, in both K influx and efflux. Changes in cell size during the volume regulatory phase are not altered by 10-4 M ouabain, although this concentration of ouabain does change the cellular cation content. The response is independent of any effect of norepinephrine. The changes in cell size during the volume regulatory phase are discussed as the product of a volume controlling mechanism identical in principle to the one reported in the previous paper which controls cell volume in hypotonic media. Similarly, this mechanism can regulate cell size, when the Na-K exchange, ouabain-inhibitable pump mechanism is blocked.

1980 ◽  
Vol 239 (6) ◽  
pp. F571-F577 ◽  
Author(s):  
M. A. Linshaw

Renal tubule cell volume is thought to be kept constant by a cation pump. Ouabain, by inhibiting Na+-K+-ATPase, blocks cation transport with resultant cell swelling, but the degree of swelling is less than expected were active cation transport completely inhibited. Although the relatively rigid tubule basement membrane may limit swelling of ouabain-treated tubules, some investigators have alternatively postulated that an energy-dependent ouabain-insensitive cation pump regulates cell size. This notion derives from studies of renal cortical slices in which metabolic inhibitors such as 2,4-dinitrophenol (DNP) cause more swelling than ouabain. We blocked cellular metabolism of isolated rabbit proximal straight tubules by adding metabolic inhibitors to or removing acetate and glucose (energy substrate) from the bathing medium and evaluated subsequent changes in cell size by measuring outer diameter of nonperfused tubules. In isotonic medium, cell volume increased 36% with addition of 10(-4) M ouabain, 40% with 10(-2) M DNP, 46% with 10(-3) M cyanide, 39% with ouabain + DNP + cyanide, and 37% with removal of bath substrate (P = NS). We conclude that renal tubule cell volume is not regulated by a unique-ouabain-insensitive cation pump.


1974 ◽  
Vol 64 (4) ◽  
pp. 393-412 ◽  
Author(s):  
Floyd M. Kregenow ◽  

Previous publications have described a "volume controlling mechanism" in duck erythrocytes that returns both enlarged and shrunken cells to their original isotonic volume. Enlarged cells return to their original size by readjusting their K content. To study the specificity of this aspect of the mechanism for K, we prepared enlarged cells with various Na and K contents. Only cells containing a high K content resume their original size in the standard isotonic medium. The process of regulation resembles that described above. In contrast, cells containing a high Na content fail to reestablish this volume, but shrink instead until they reach a limiting minimal volume (four-fifths of normal). Here, another mechanism, the cation pump rather than the volume controlling mechanism, removes Na and is responsible for the changes in cell size. Enlarged cells with an intermediate Na and K content utilize both mechanisms to reduce their cation content. Only if Na is prevented from leaving the cell and sufficient K is present initially, will these cells reestablish their original size. These studies demonstrate that the cation pump and volume controlling mechanism function independently and, when cells enlarge, only K can effectively traverse the pathway associated with the volume controlling mechanism. This route differs from the one used by the cation pump to eject Na.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Michele Bonus ◽  
Dieter Häussinger ◽  
Holger Gohlke

Abstract Liver cell hydration (cell volume) is dynamic and can change within minutes under the influence of hormones, nutrients, and oxidative stress. Such volume changes were identified as a novel and important modulator of cell function. It provides an early example for the interaction between a physical parameter (cell volume) on the one hand and metabolism, transport, and gene expression on the other. Such events involve mechanotransduction (osmosensing) which triggers signaling cascades towards liver function (osmosignaling). This article reviews our own work on this topic with emphasis on the role of β1 integrins as (osmo-)mechanosensors in the liver, but also on their role in bile acid signaling.


1976 ◽  
Vol 231 (5) ◽  
pp. 1568-1572 ◽  
Author(s):  
M DiGirolamo ◽  
JL Owens

Epididymal adipose tissue composition and adipocyte water content were studied in male rats during growth and development of spontaneous obesity. The data show that a highly significant positive correlation exists between fat-cell volume and intracellular water space (IWS) (r=.967, P less than .001). Intracellular water, expressed as picoliters per fat cell, varied from 1.5-2 in small fat cells (mean vol, 30-50 pl) to 9-10 in large cells (800-1,000 pl). When expressed as percent of fat-cell volume, IWS varied from 5-7% in the small fat cells to 1-1.3% in the large ones. Total adipose tissue water continued to increase with increasing adipose mass. Similarly, total adipocyte water increased with enlarging cell size and tissue mass. The contribution of total adipocyte water (as contrasted to that of nonadipocyte water) to total tissue water, however, was found to be limited (less than 23%) and to decline progressively with adipose mass expansion.


1977 ◽  
Vol 69 (5) ◽  
pp. 537-552 ◽  
Author(s):  
PM Cala

The nucleated high K, low Na red blood cells of the winter flounder demonstrated a volume regulatory response subsequent to osmotic swelling or shrinkage. During volume regulation the net water flow was secondary to net inorganic cation flux. Volume regulation the net water flow was secondary to net inorganic cation flux. Volume regulation after osmotic swelling is referred to as regulatory volume decrease (RVD) and was characterized by net K and water loss. Since the electrochemical gradient for K is directed out of the cell there is no need to invoke active processes to explain RVD. When osmotically shrunken, the flounder erythrocyte demonstrated a regulatory volume increase (RVI) back toward control cell volume. The water movements characteristic of RVI were a consequence of net cellular NaCl and KCl uptake with Na accounting for 75 percent of the increase in intracellular cation content. Since the Na electrochemical gradient is directed into the cell, net Na uptake was the result of Na flux via dissipative pathways. The addition of 10(-4)M ouabain to suspensions of flounder erythrocytes was without effect upon net water movements during volume regulation. The presence of ouabain did however lead to a decreased ration of intracellular K:Na. Analysis of net Na and K fluxes in the presence and absence of ouabain led to the conclusion that Na and K fluxes via both conservative and dissipative pathways are increased in response to osmotic swelling or shrinkage. In addition, the Na and K flux rate through both pump and leak pathways decreased in a parallel fashion as cell volume was regulated. Taken as a whole, the Na and K movements through the flounder erythrocyte membrane demonstrated a functional dependence during volume regulation.


2021 ◽  
pp. 0021955X2098715
Author(s):  
Cosimo Brondi ◽  
Ernesto Di Maio ◽  
Luigi Bertucelli ◽  
Vanni Parenti ◽  
Thomas Mosciatti

This study investigates the effect of liquid-type organofluorine additives (OFAs) on the morphology, thermal conductivity and mechanical properties of rigid polyurethane (PU) and polyisocyanurate (PIR) foams. Foams were characterized in terms of their morphology (density, average cell size, anisotropy ratio, open cell content), thermal conductivity and compressive as well as flexural properties. Based on the results, we observed that OFAs efficiently reduced the average cell size of both PU and PIR foams, leading to improved thermal insulating and mechanical properties.


1977 ◽  
Vol 233 (4) ◽  
pp. F325-F332
Author(s):  
M. A. Linshaw ◽  
F. B. Stapleton ◽  
F. E. Cuppage ◽  
J. J. Grantham

Renal tubule cell volume is thought to be kept constant by a cation pump. When active transport is blocked, intracellular impermeant solutes cause cells to swell. Cell size is then determined by transmembrane hydrostatic and colloid osmotic forces. We studied the importance of passive transmembrane forces in determining cell size in isolated rabbit proximal straight tubules (PST). We blocked active solute transport with ouabain and evaluated subsequent changes in cell size by measuring outer diameter of nonperfused tubules. Tubules in a ouabain and 6 g/100 ml protein bath swelled only 40% above control. However, removal of the tubule basement membrane with collagenase dissipated a transmembrane hydrostatic pressure and caused more swelling. Final cell volume was determined largely by bath protein concentration. Tubules in ouabain and collagenase swelled enormously in hyponcotic protein, moderately in isoncotic protein, and could be shrunk below control in hyperoncotic protein. Intracellular colloid osmotic pressure was estimated to exceed 38 cmH20. We conclude that hydrostatic and colloid osmotic forces are major determinants of cell size in isolated PST treated with ouabain.


1989 ◽  
Vol 257 (5) ◽  
pp. R982-R988
Author(s):  
W. H. Dantzler

Net fluid absorption (Jv), cell volume, and cell membrane area have been studied in isolated, perfused snake (Thamnophis spp.) proximal tubules. With Na+ in both perfusate and bathing medium, Jv averages approximately 0.9 nl.min-1.mm-1. When choline replaces Na+ in perfusate, Jv nearly ceases. When choline also replaces Na+ in bathing medium, so that both solutions are identical, Jv returns to the control rate. The results are the same when tetramethylammonium replaces Na+, when sucrose replaces Na+ and the equivalent amount of Cl-, and when methyl sulfate replaces Cl- alone. However, when Li+ replaces Na+ in perfusate alone or in both perfusate and bathing medium, Jv is unchanged. Jv at control rates is isosmotic and can be partially inhibited by cold and cyanide. When choline replaces Na+ in perfusate and bathing medium, cell volume doubles, and intercellular space volume nearly quintuples. The areas of the lateral and apical cell membranes also approximately double, so that the surface area-to-volume ratio remains constant. These morphological changes in the absence of Na+ occur concomitantly with maintenance of Jv, suggesting that they may play a permissive role in such maintenance.


2019 ◽  
Vol 5 (12) ◽  
pp. eaax9484 ◽  
Author(s):  
Kristian Parey ◽  
Outi Haapanen ◽  
Vivek Sharma ◽  
Harald Köfeler ◽  
Thomas Züllig ◽  
...  

Respiratory complex I is a redox-driven proton pump, accounting for a large part of the electrochemical gradient that powers mitochondrial adenosine triphosphate synthesis. Complex I dysfunction is associated with severe human diseases. Assembly of the one-megadalton complex I in the inner mitochondrial membrane requires assembly factors and chaperones. We have determined the structure of complex I from the aerobic yeast Yarrowia lipolytica by electron cryo-microscopy at 3.2-Å resolution. A ubiquinone molecule was identified in the access path to the active site. The electron cryo-microscopy structure indicated an unusual lipid-protein arrangement at the junction of membrane and matrix arms that was confirmed by molecular simulations. The structure of a complex I mutant and an assembly intermediate provide detailed molecular insights into the cause of a hereditary complex I–linked disease and complex I assembly in the inner mitochondrial membrane.


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