Effect of metabolic inhibitors on renal tubule cell volume

1980 ◽  
Vol 239 (6) ◽  
pp. F571-F577 ◽  
Author(s):  
M. A. Linshaw
Keyword(s):  
Cell Volume ◽  
Cell Size ◽  
Renal Tubule ◽  
Cation Transport ◽  
Metabolic Inhibitors ◽  
Cell Swelling ◽  
Tubule Cell ◽  
Bathing Medium ◽  
Cation Pump ◽  
Renal Tubule Cell

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.

Effect of basement membrane and colloid osmotic pressure on renal tubule cell volume

1977 ◽  
Vol 233 (4) ◽  
pp. F325-F332
Author(s):  
M. A. Linshaw ◽  
F. B. Stapleton ◽  
F. E. Cuppage ◽  
J. J. Grantham
Keyword(s):  
Basement Membrane ◽  
Osmotic Pressure ◽  
Cell Volume ◽  
Cell Size ◽  
Renal Tubule ◽  
Colloid Osmotic Pressure ◽  
Outer Diameter ◽  
Tubule Cell ◽  
Cation Pump ◽  
Renal Tubule Cell

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.

Effect of ouabain and colloid osmotic pressure on renal tubule cell volume

1978 ◽  
Vol 235 (5) ◽  
pp. F480-F491
Author(s):  
M. A. Linshaw ◽  
F. B. Stapleton
Keyword(s):  
Osmotic Pressure ◽  
Cell Volume ◽  
Renal Tubule ◽  
Colloid Osmotic Pressure ◽  
Cell Swelling ◽  
Outer Diameter ◽  
Tubule Cell ◽  
Fluid Flux ◽  
Renal Tubule Cell ◽  
Collecting Tubules

Proximal renal tubule cell volume increases in ouabain but cell swelling is limited by the tubule basement membrane (TBM) and the colloid osmotic pressure from the bath protein. We compared the effect of ouabain, external protein concentration, and TBM on cell volume of proximal convoluted (PCT), proximal straight (PST), and cortical collecting tubules (CCT). We blocked active solute transport with ouabain and evaluated cell size by measuring the outer diameter of nonperfused tubules. Proximal tubules in ouabain swelled 35–40% in isoncotic medium and 20–25% further in hyponcotic medium (0.3 g/100 ml albumin), but PCT swelled faster than PST. The CCT swelled minimally in similar mediums, indicating pronounced heterogeneity in the response of cortical nephron segments to ouabain. In the presence of ouabain, all tubules swelled extensively when we removed the TBM with collagenase. In the hyponcotic medium fluid flux across the peritubular membrane was 0.081, 0.049, and 0.030 nl/min per mm tubule length for PCT, PST, and CCT, respectively. The rates of fluid flux in PCT and PST were proportional to estimates of the respective basolateral surface areas. We suggest that differences in swelling rates between proximal segments reflect variations in surface area rather than intrinsic peritubular membrane permeability to solute and water.

scholarly journals The Effect of Chronic Progressive Nephropathy on the Incidence of Renal Tubule Cell Neoplasms in Control Male F344 Rats

2002 ◽  
Vol 30 (6) ◽  
pp. 681-686 ◽  
Author(s):  
John C. Seely ◽  
Joseph K. Haseman ◽  
Abraham Nyska ◽  
Douglas C. Wolf ◽  
Jeffrey I. Everitt ◽  
...  
Keyword(s):  
Renal Tubule ◽  
Tubule Cell ◽  
Control Male ◽  
Renal Tubule Cell ◽  
F344 Rats ◽  
Male F344 Rats

scholarly journals The Response of Duck Erythrocytes to Hypertonic Media

1971 ◽  
Vol 58 (4) ◽  
pp. 396-412 ◽  
Author(s):  
Floyd M. Kregenow
Keyword(s):  
Cell Volume ◽  
Cell Size ◽  
Hypertonic Solution ◽  
Electrochemical Gradient ◽  
Cell Content ◽  
Bathing Medium ◽  
Instantaneous Phase ◽  
Controlling Mechanism ◽  
Pump Mechanism ◽  
The One

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.

Potassium-induced cell swelling in Necturus gallbladder epithelium

1988 ◽  
Vol 254 (5) ◽  
pp. C643-C650 ◽  
Author(s):  
C. W. Davis ◽  
A. L. Finn
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Basolateral Membrane ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Gallbladder Epithelium ◽  
Bathing Medium ◽  
Necturus Gallbladder ◽  
Per Se ◽  
Cl Conductance

In Necturus gallbladder epithelium, elevation of mucosal K+ to 95 mM in the presence of 10 mM Na+ resulted in cell swelling at a rate of 3.2% original volume per minute, followed by volume-regulatory shrinking. When Na+ was completely removed from or when amiloride (10(-4) M) was added to the mucosal medium, K+-induced cell swelling was abolished. In the presence of 10 mM Na+, 1 mM Ba2+ abolished and substitution of mucosal Cl- by NO-3 had no effect on K+-induced swelling. Thus solute entry following elevation of mucosal K+ is effected by separate K+ and Cl- pathways. Furthermore, substitution of 95 mM K+ for Na+ in the mucosal bathing medium leads to the development of a Cl- conductance in the basolateral membrane as long as some Na+ remains in the medium. However, cell swelling induced by mucosal dilution does not lead to the appearance of a Cl- conductance. Thus the activation of this conductance requires both swelling and membrane depolarization. These results show that 1) high mucosal K+ leads to cell swelling due to the entry of Cl- along with K+ and the Cl- can enter across either membrane, 2) the Cl- pathways require the presence of mucosal Na+, and 3) cell volume regulation is activated by an increase in volume per se, i.e., a hyposmotic exposure is not required for volume regulation to occur.

Using Hyperactive Antifreeze Proteins To Supercool A Renal Tubule Cell Line

Cryobiology ◽  
2021 ◽  
Vol 103 ◽  
pp. 181
Author(s):  
Heather E. Tomalty ◽  
Virginia K. Walker ◽  
Peter L. Davies
Keyword(s):  
Cell Line ◽  
Renal Tubule ◽  
Antifreeze Proteins ◽  
Tubule Cell ◽  
Renal Tubule Cell
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