GSH depletion, K-Cl cotransport, and regulatory volume decrease in high-K/high-GSH dog red blood cells

2001 ◽  
Vol 281 (6) ◽  
pp. C2003-C2009 ◽  
Author(s):  
Hiroshi Fujise ◽  
Kazunari Higa ◽  
Tomomi Kanemaru ◽  
Miwa Fukuda ◽  
Norma C. Adragna ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Redox System ◽  
Glutathione S Transferase ◽  
High Potassium ◽  
High K ◽  
Protein Thiols ◽  
Volume Decrease

Thiol reagents activate K-Cl cotransport (K-Cl COT), the Cl-dependent and Na-independent ouabain-resistant K flux, in red blood cells (RBCs) of several species, upon depletion of cellular glutathione (GSH). K-Cl COT is physiologically active in high potassium (HK), high GSH (HG) dog RBCs. In this unique model, we studied whether the same inverse relationship exists between GSH levels and K-Cl COT activity found in other species. The effects of GSH depletion by three different chemical reactions [nitrite (NO2)-mediated oxidation, diazene dicarboxylic acid bis- N, N-dimethylamide (diamide)-induced dithiol formation, and glutathione S-transferase (GST)-catalyzed conjugation of GSH with 1-chloro-2,4-dinitrobenzene (CDNB)] were tested on K-Cl COT and regulatory volume decrease (RVD). After 85% GSH depletion, all three interventions stimulated K-Cl COT half-maximally with the following order of potency: diamide > NO2 > CDNB. Repletion of GSH reversed K-Cl COT stimulation by 50%. Cl-dependent RVD accompanied K-Cl COT activation by NO2 and diamide. K-Cl COT activation at concentration ratios of oxidant/GSH greater than unity was irreversible, suggesting either nitrosothiolation, heterodithiol formation, or GST-mediated dinitrophenylation of protein thiols. The data support the hypothesis that an intact redox system, rather than the absolute GSH levels, protects K-Cl COT activity and cell volume regulation from thiol modification.

K(+)-Cl- cotransport and volume regulation in the light and the dense fraction of high-K+ dog red blood cells

1997 ◽  
Vol 273 (3) ◽  
pp. R991-R998 ◽  
Author(s):  
H. Fujise ◽  
K. Abe ◽  
M. Kamimura ◽  
H. Ochiai
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Divalent Cations ◽  
Regulatory Volume Decrease ◽  
Marker Enzyme ◽  
High K ◽  
Dense Fraction ◽  
Glucose 6 Phosphate Dehydrogenase ◽  
Volume Decrease ◽  
Light Cells

We examined a chloride (Cl-)-dependent K+ transport (K(+)-Cl- cotransport) and regulatory volume decrease in dog red blood cells with high K+, low Na+, and high glutathione (GSH) content (HK/HG) due to the presence of an Na(+)-K+ pump. The HK/HG cells were separated according to their density, and the age-marker enzyme activities, such as glucose-6-phosphate dehydrogenase and cholinesterase, were determined. Unexpectedly, we found that young cells were heavier (more dense) and smaller in size compared with the old cells, which were lighter (less dense) and larger. The K(+)-Cl- cotransport was nearly 10-fold higher in the most dense cells, representing a 12% fraction of the total population compared with the lightest cohort. Although K(+)-Cl- cotransport in both the dense and the light cells was activated by N-ethylmaleimide, swelling and depletion of cellular divalent cations and the activation of the transport in the dense cells was greater. Both the dense and light cells regulated their volume when they were isosmotically swollen. Therefore, the lower activity of K(+)-Cl- cotransport might not explain the relative large volume in old HK/HG cells. The concentration of GSH and glutamate was higher in the light cells. Thus the higher the GSH and glutamate concentration, the greater the cell volume and the lower the K(+)-Cl- cotransport.

scholarly journals Volume regulation by Amphiuma red blood cells. The membrane potential and its implications regarding the nature of the ion-flux pathways.

1980 ◽  
Vol 76 (6) ◽  
pp. 683-708 ◽  
Author(s):  
P M Cala
Keyword(s):  
Membrane Potential ◽  
Alkali Metal ◽  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Cells ◽  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Ion Flux ◽  
Regulatory Response

After osmotic perturbation, the red blood cells of Amphiuma exhibited a volume-regulatory response that returned cell volume back to or toward control values. After osmotic swelling, cell-volume regulation (regulatory volume decrease; RVD) resulted from net cellular loss of K, Cl, and osmotically obliged H2O. In contrast, the volume-regulatory response to osmotic shrinkage (regulatory volume increase; RVI) was characterized by net cellular uptake of Na, Cl, and H2O. The net K and Na fluxes characteristic of RVD and RVI are increased by 1-2 orders of magnitude above those observed in studies of volume-static control cells. The cell membrane potential of volume-regulating and volume-static cells was measured by impalement with glass microelectrodes. The information gained from the electrical and ion-flux studies led to the conclusion that the ion fluxes responsible for cell-volume regulation proceed via electrically silent pathways. Furthermore, it was observed that Na fluxes during RVI were profoundly sensitive to medium [HCO3] and that during RVI the medium becomes more acid, whereas alkaline shifts in the suspension medium accompany RVD. The experimental observations are explained by a model featuring obligatorily coupled alkali metal-H and Cl-HCO3 exchangers. The anion- and cation-exchange pathways are separate and distinct yet functionally coupled via the net flux of H. As a result of the operation of such pathways, net alkali metal, Cl, and H2O fluxes proceed in the same direction, whereas H and HCO3 fluxes are cyclic. Data also are presented that suggest that the ion-flux pathways responsible for cell-volume regulation are not activated by changes in cell volume per se but by some event associated with osmotic perturbation, such as changes in intracellular pH.

scholarly journals Evidence of Coordinated and Adjustable Osmolytes Movements Following Hyposmotic Swelling in Rainbow Trout Red Blood Cells

2021 ◽  
Vol 55 (S1) ◽  
pp. 185-195
Author(s):  
Valérie Maxime ◽  
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Blood Cells ◽  
Volume Regulation ◽  
Rapid Change ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Gravimetric Method ◽  
Ph Control ◽  
Na Uptake

BACKGROUND/AIMS: The osmolytes involved in the volume regulation of hyposmotically-swollen fish cells are well identified. However, if a coordination and adjustments of their fluxes are obvious, few studies have clearly illustrated these aspects. METHODS: Trout red blood cells volume variations were estimated from water contents obtained by a gravimetric method. Intracellular K+ and Na+ contents, and Cl- content of haemolysed cells were determined by photometry and colorimetry, respectively. The taurine contribution to cell volume regulation was calculated from the net changes of water, K+, Cl- and Na+ contents. The intracellular pH was calculated from the chloride distribution across the cells membranes according to the Donnan equilibrium. RESULTS: Cells responses to a rapid change (from 296 to 176 mOsm.kg-1)
of the saline osmolality were examined in three conditions designed to not impact (Hypo. I)
or to reduce the K+ (Hypo. II) and Cl- (Hypo. III) contributions to the volume regulation. Hypo. I condition caused an immediate increase in water content, followed by a 90 min. full regulation, concomitant with gradual lowering of K+ and Cl- contents and a surprising increase in Na+ content. Hypo. II and III conditions showed a partial and complete volume regulation, respectively. This was made possible by an increase in the taurine involvement. These experiments allowed to confirm that K+ and Cl- were released via KCl cotransport and by separate channels. The comparison of Hypo. I and III conditions led to the observation that the partially amiloride-sensitive Na+ influx is proportional to the taurine efflux; the latter being sustained mainly by a Na+/taurine cotransport. The Hypo. II condition was suitable for the (Na+/K+)ATPase activity inhibition. This effect could explain the observed lack of Na+ uptake, the consecutive depletion of intracellular taurine stock and the incomplete volume regulation. Finally, the results support the importance of taurine in pH control under Hypo. I (physiologic) condition. The alkalosis observed in Hypo. II and III conditions were the consequences of changes in the salines compositions, not of physiologic adjustments. CONCLUSION: The regulatory volume decrease process of trout RBCs is complex and adjustable through coordinated osmolytes movements. The obliged decrease in K+ and/or Cl- contributions stimulates taurine and Na+ pathways. This study highlights the importance of taurine as a compensatory variable in cell volume regulation and explains for the first time the significance of the Na+ uptake during this process

Regulatory volume decrease in northern fur seal (Callorhinus ursinus) red blood cells

2006 ◽  
Vol 16 (1) ◽  
pp. 61-63
Author(s):  
H. Ochiai ◽  
N. Hishiyama ◽  
K. Higa ◽  
K. Koyama ◽  
M. Seita ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Regulatory Volume Decrease ◽  
Callorhinus Ursinus ◽  
Northern Fur Seal ◽  
Fur Seal ◽  
Volume Decrease

Potassium conductance activated during regulatory volume decrease by mudpuppy red blood cells

1996 ◽  
Vol 270 (4) ◽  
pp. R801-R810
Author(s):  
L. J. Bergeron ◽  
A. J. Stever ◽  
D. B. Light
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Enhanced Recovery ◽  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
K Channel ◽  
Ionophore A23187 ◽  
Patch Clamp Technique ◽  
Extracellular Medium ◽  
Volume Decrease

The cellular basis of regulatory volume decrease (RVD) by mudpuppy (Necturus maculosus) red blood cells (RBCs) was examined. Volume regulation was inhibited by replacing extracellular Na+ with K+. In contrast, addition of gramicidin (5 microM) to the extracellular medium enhanced RVD. The K(+)-channel blocker quinine (1 mM) also inhibited RVD, and this inhibition was reversed by gramicidin (5 microM). In addition, a 0 Ca(2+)-EGTA Ringer blocked RVD, whereas the Ca2+ ionophore A23187 ( microM) enhanced recovery of cell volume. The stretch-activated ion channel antagonist gadolinium (10 microM) inhibited RVD, and this effect was reversed by A23187 (2 microM). Furthermore, the calmodulin inhibitors pimozide (10 microM) and N-(6-aminohexyl)-5-chloro-1-napthalene-sulfonamide (0.1 mM) blocked RVD, and this inhibition was reversed with gramicidin (5 microM). Consistent with these findings, a K(+)-selective membrane conductance was activated by exposing RBCs to a 0.5x Ringer solution (observed with the whole cell patch clamp technique). This conductance was inhibited by quinine (1 mM), gadolinium (10 microM), and pimozide (10 microM). These results indicate that cell swelling activates a K+ conductance by a Ca(2+)-calmodulin-dependent mechanism and that this channel mediates K+ loss during RVD.

scholarly journals Regulatory volume decrease in carp red blood cells: mechanisms and oxygenation-dependency of volume-activated potassium and amino acid transport

1995 ◽  
Vol 198 (1) ◽  
pp. 155-165 ◽  
Author(s):  
F Jensen
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
Organic Osmolytes ◽  
Osmotic Swelling ◽  
Original Cell ◽  
Sufficient Stimulus ◽  
K Release ◽  
Volume Decrease

Hypo-osmotic swelling of carp red blood cells (RBCs) induced a regulatory volume decrease (RVD), which restored the original cell volume within 140 min in oxygenated RBCs, whereas volume recovery was incomplete in deoxygenated RBCs. The complete RVD in oxygenated RBCs resulted from a sustained volume-activated release of K+, Cl- and amino acids (AAs). In the absence of ouabain, the cells also lost Na+ as released K+ was partially regained via the Na+/K+ pump. Inorganic osmolytes contributed approximately 70 %, and organic osmolytes approximately 30 %, to the RVD of oxygenated RBCs. Oxygenation in isotonic medium per se activated a K+ efflux from the RBCs. Hypo-osmotic cell swelling stimulated an additional K+ release. The oxygenation-activated and the volume-activated K+ efflux were both inhibited by DIDS and by the replacement of Cl- with NO3-, showing that both types of K+ efflux were Cl--dependent and probably occurred via the same K+/Cl- cotransport mechanism. Once activated by oxygenation, the K+/Cl- cotransport was further stimulated by cell swelling. Deoxygenation inactivated the oxygenation-induced Cl--dependent K+ release and cell swelling was not a sufficient stimulus to reactivate it significantly. In deoxygenated RBCs, the volume-induced K+ release was transient and primarily Cl--independent and, in the absence of ouabain, the cell K+ content recovered towards control values via the Na+/K+ pump. The Cl--independent K+ efflux seemed to involve K+/H+ exchange, but other transport routes also participated. Swelling-activated AA release differed in kinetics between oxygenated and deoxygenated RBCs but was important for RVD at both oxygenation degrees. Approximately 70 % of the AA release was inhibited by DIDS and substitution of NO3- for Cl- produced a 50 % inhibition, suggesting that the AA permeation was partly Cl--dependent. In oxygenated RBCs, a reduction in pH lowered the volume-activated Cl--dependent K+ efflux but not the AA efflux. In deoxygenated RBCs, the acute volume-stimulated K+ and AA release were both increased by acidification. The data are discussed in relation to possible transducer mechanisms and physiological implications.

Hypoxia inhibits the regulatory volume decrease in red blood cells of common frog ( Rana temporaria )

2018 ◽  
Vol 219-220 ◽  
pp. 44-47 ◽  
Author(s):  
Aleksandra Y. Andreyeva ◽  
Elizaveta A. Skverchinskaya ◽  
Stepan Gambaryan ◽  
Aleksander A. Soldatov ◽  
Igor V. Mindukshev
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Rana Temporaria ◽  
Regulatory Volume Decrease ◽  
Common Frog ◽  
Frog Rana Temporaria ◽  
Volume Decrease

Protein Kinase C and Regulatory Volume Decrease in Mudpuppy Red Blood Cells

1998 ◽  
Vol 166 (2) ◽  
pp. 119-132 ◽  
Author(s):  
D.B. Light ◽  
M.R. Adler ◽  
J.K. Ter Beest ◽  
S.A. Botsford ◽  
R.T. Gronau
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Regulatory Volume Decrease ◽  
Kinase C ◽  
Volume Decrease
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