Effect of barium on cell volume regulation in rabbit proximal straight tubules

1985 ◽  
Vol 249 (1) ◽  
pp. F20-F27 ◽  
Author(s):  
P. A. Welling ◽  
M. A. Linshaw ◽  
L. P. Sullivan

Rabbit proximal straight tubules swell abruptly when exposed to hypotonic medium but then shrink in a few minutes as they approach their base-line volume following loss of solute and water. Potassium, the major intracellular cation, as well as sodium, is lost during this process. In the present experiments, we studied hypotonic cell volume regulation in the presence of barium, an agent reported to decrease potassium permeability. Exposure to BaCl2 significantly prolonged hypotonic volume recovery in a dose-dependent manner. Tubules depleted of potassium and loaded with sodium chloride by exposure to 10(-4) M ouabain for 1 h swelled osmometrically and subsequently volume regulated in dilute medium. Volume regulation in such tubules is a consequence of transbasement membrane hydrostatic forces. By contrast, tubules similarly loaded with sodium, but also exposed to 10(-3) M BaCl2, volume regulated only minimally in dilute medium, suggesting BaCl2 might also affect sodium movement. However, hypotonic volume regulation was restored in sodium-loaded BaCl2-treated tubules when cells were more effectively depleted of potassium by incubation in 0-mM potassium medium. We conclude that barium retards hypotonic volume regulation primarily because of its effect on potassium movement.

1977 ◽  
Vol 232 (1) ◽  
pp. F42-F49 ◽  
Author(s):  
J. J. Grantham ◽  
C. M. Lowe ◽  
M. Dellasega ◽  
B. R. Cole

The intracellular content of K and Na was measured in isolated nonperfused proximal straight renal tubules (PST) in order to determine the mode of cell volume regulation in hypotonic bathing media. Immersion in hypotonic medium caused PST to lose K and Na (with anions) in a magnitude sufficient to account for the regulation of cell volume. Hypothermia (10 degrees C) blocked cell volume regulation in hypotonic medium by promoting net accumulation of Na, although K loss was equivalent to that observed at 37 degrees C. Ouabain (10(-5) M) caused rapid loss of cell K and gain of Na in an isotonic bath, but the glycoside did not inhibit the subsequent adjustment of cell volume in hypotonic medium. In hypotonic medium ouabain-treated tubules lost Na, but not K, to account for hypotonic volume adjustment of PST in ouabain. We conclude that proximal straight tubules extrude electrolytes (K, Na, and anions) in the adjustment of cell volume in hypotonic media; in normal tubules K and Na are lost whereas Na moves primarily in ouabain-treated tubules. The adjustment of size through the extrusion of intracellular solutes in dilutional states appears to be a general property of mammalian cells.


1990 ◽  
Vol 259 (6) ◽  
pp. F950-F960 ◽  
Author(s):  
N. A. McCarty ◽  
R. G. O'Neil

The mechanism underlying the activation of hypotonic cell volume regulation was studied in rabbit proximal straight tubule (PST). When isolated non-perfused tubules were exposed to hypotonic solution, cells swelled rapidly and then underwent a regulatory volume decrease (RVD). The extent of regulation after swelling was highly dependent on extracellular Ca concentration ([Ca2+]o), with a half-maximal inhibition (K1/2) for [Ca2+]o of approximately 100 microM. RVD was blocked by the Ca-channel blockers verapamil, lanthanum, and the dihydropyridines (DHP) nifedipine and nitrendipine, implicating voltage-activated Ca channels in the RVD response. Using the fura-2 fluorescence-ratio technique, we observed that cell swelling caused a sustained rise in intracellular Ca ([Ca2+]i) only when [Ca2+]o was normal (1 mM) but not when [Ca2+]o was low (1-10 microM). Furthermore, external Ca was required early on during swelling to induce RVD. If RVD was initially blocked by reducing [Ca2+]o or by addition of verapamil during hypotonic swelling, volume regulation could only be restored by subsequently inducing Ca entry within the first 1 min or less of exposure to hypotonic solution. These data indicate a "calcium window" of less than 1 min, during which RVD is sensitive to Ca, and that part of the Ca-dependent mechanism responsible for achieving RVD undergoes inactivation after swelling. It is concluded that RVD in rabbit PST is modulated by Ca via a DHP-sensitive mechanism in a time-dependent manner.


2011 ◽  
Vol 437 (1) ◽  
pp. 79-81 ◽  
Author(s):  
E. I. Solenov ◽  
A. V. Ilyaskin ◽  
G. S. Baturina ◽  
D. A. Medvedev ◽  
A. P. Ershov ◽  
...  

2011 ◽  
Vol 436 (1) ◽  
pp. 13-15 ◽  
Author(s):  
E. I. Solenov ◽  
G. S. Baturina ◽  
A. V. Ilyaskin ◽  
L. Ye. Katkova ◽  
L. N. Ivanova

1979 ◽  
Vol 236 (3) ◽  
pp. F226-F231
Author(s):  
M. Paillard ◽  
F. Leviel ◽  
J. P. Gardin

The regulation of cell volume was studied in separated renal tubules (SRT) whose basement membrane had been removed by collagenase. Regulation occurred when SRT were immersed in a hypotonic medium, the increase in cellular water content being half that expected in the absence of regulation. Regulation was immediate, with no initial swelling, and was accompanied by a loss of NaCl, with no change in cellular K. This regulation was eliminated by 10(-3) M ouabain. We conclude that: 1) Cell volume regulation which occurs in a hypotonic medium is due to an immediate loss of NaCl. 2) Loss of NaCl might be due to blocking of the net passive NaCl entry into the cells resulting from the drop in the transmembrane NaCl electrochemical gradient. The high membrane sodium permeability, probably located on the luminal side of the tubular cells, might explain why regulation was instantaneous. 3) Elimination of volume regulation by ouabain suggests there is no need to assume that a ouabain-insensitive pump regulates cell volume.


1980 ◽  
Vol 238 (6) ◽  
pp. F491-F498 ◽  
Author(s):  
M. A. Linshaw ◽  
J. J. Grantham

Proximal straight tubules (S2 segments) swell rapidly in hypotonic media, but within a few minutes their volume returns toward control levels due to extrusion of K, Na, Cl, and water from the cytoplasm. In the present studies we determined the extent to which hydrostatic pressure (derived from the elastic tubule basement membrane (TBM) as the tubule enlarged in hypotonic medium) contributed to the regulation of cell volume. Removal of the TBM by collagenase had no effect on cell volume regulation in otherwise normal tubules. By contrast, tubules treated with ouabain, though they appeared to regulate their volumes in hypotonic media, were unable to do so in the presence of glycoside if the TBM had been removed with collagenase. This latter result is interpreted to show that hydrostatic pressure generated by extension of the TBM can cause “apparent” volume regulation when the sodium pump is blocked by ouabain. We conclude that normal proximal renal tubules regulate cell volume in hypotonic solutions by mechanisms that are dependent on the normal operation of the classical sodium pump.


Sign in / Sign up

Export Citation Format

Share Document