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.

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 Volume regulation by flounder red blood cells in anisotonic media

1977 ◽  
Vol 69 (5) ◽  
pp. 537-552 ◽  
Author(s):  
PM Cala
Keyword(s):  
Red Blood Cells ◽  
Cell Volume ◽  
Water Flow ◽  
Blood Cells ◽  
Volume Regulation ◽  
Control Cell ◽  
Regulatory Volume Decrease ◽  
Electrochemical Gradient ◽  
Osmotic Swelling ◽  
Inorganic Cation

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.

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.

Swelling-activated K+ transport via two functionally distinct pathways in eel erythrocytes

1996 ◽  
Vol 270 (1) ◽  
pp. R61-R70 ◽  
Author(s):  
J. D. Bursell ◽  
K. Kirk
Keyword(s):  
Regulatory Volume Decrease ◽  
Anguilla Anguilla ◽  
Cell Swelling ◽  
European Eel ◽  
Pharmacological Properties ◽  
Osmotic Swelling ◽  
Diverse Range ◽  
K Transport ◽  
Volume Decrease ◽  
In Cells

Following osmotic swelling, erythrocytes from the European eel, Anguilla anguilla, underwent a regulatory volume decrease. This was prevented by replacement of Na+ with K+ in the suspending medium, consistent with a role for the (normally outward) electrochemical K+ gradient in the volume-regulatory response. The effect of cell swelling on K- transport in these cells was investigated using 86Rb+ as a tracer for K+. Osmotic swelling resulted in an increase in ouabain-insensitive K+ transport that was highest for cells in Cl- and Br- media but which was also significant in I- and NO3- media. Treatment of eel erythrocytes suspended in isotonic Cl- or Br- (but not I- or NO3-) media with the sulfhydryl reagent N-ethylmaleimide (NEM) resulted in a large increase in K+ transport. A quantitative comparison of the pharmacological properties of the “Cl(-)-dependent” NEM-activated pathway with those of the “Cl(-)-independent” pathway mediating swelling-activated K+ transport in cells in Cl(-)-free (NO3- containing) media showed there to be significant differences between them. By contrast, the pharmacological properties of the Cl(-)-independent swelling-activated K+ pathway were indistinguishable from those of the pathway responsible for the swelling-activated transport of taurine, the major organic osmolyte in these cells. A pharmacological analysis of ouabain-insensitive K+ transport in cells swollen in a hypotonic Cl(-)-containing medium showed there to be two components, one with the characteristics of the NEM-activated system, the other showing the characteristics of the Cl(-)-independent swelling-activated pathway. The data are consistent with the presence of two functionally distinct swelling-activated K+ transport mechanisms in eel erythrocytes: a KCl cotransporter that is activated under isotonic conditions by NEM and a Cl(-)-independent, broad-specificity channel that accommodates a diverse range of organic and inorganic solutes.

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

Mechanisms of regulatory volume decrease in nonpigmented human ciliary epithelial cells

1995 ◽  
Vol 268 (3) ◽  
pp. C721-C731 ◽  
Author(s):  
J. S. Adorante ◽  
P. M. Cala
Keyword(s):  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
Ciliary Epithelium ◽  
Channel Blockers ◽  
Tetraacetic Acid ◽  
Acetoxymethyl Ester ◽  
Osmotic Swelling ◽  
Ion Efflux ◽  
Volume Recovery ◽  
Volume Decrease

To study the net solute and water efflux pathways of the ciliary epithelium we employed a cultured human NPE cell line. Because of the possible relationship between transepithelial ion and water flux and cell volume regulation, the ion efflux pathways mediating regulatory volume decrease (RVD) were investigated. Osmotic swelling of NPE cells was followed by a volume recovery. Volume recovery was K+ dependent and inhibited by K+ channel blockers such as quinine (1 mM). After osmotic swelling, a Cl(-)-dependent membrane depolarization occurred that was inhibited by Cl- channel blockers such as 5-nitro-2-(3-phenylpropylamino)benzoic acid (100 microM) or Ca2+ chelators such as ethylene glycolbis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA, 2.0 mM). Cell swelling was also accompanied by an increase in intracellular Ca2+ concentration ([Ca2+]i) of approximately 200 nM. The swelling-induced rise in [Ca2+]i and RVD were diminished in the presence of 10 microM La3+, 50 nM 12-O-tetradecanoylphorbol 13-acetate, and nominally Ca(2+)-free medium. Near total blockage of RVD occurred after pretreatment of NPE cells with Ca(2+)-free EGTA-1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) acetoxymethyl ester-containing solutions. The inhibition of RVD by EGTA-BAPTA treatment was overcome by increasing K+ conductance with gramicidin. The above findings indicate that RVD in NPE cells is mediated by separate K+ and Cl- conductances (channels). These data also show that swelling-induced increases in [Ca2+]i help modulate net ion efflux during regulation.

Tyrosine kinase inhibition affects skate anion exchanger isoform I alterations after volume expansion

2005 ◽  
Vol 288 (4) ◽  
pp. R885-R890 ◽  
Author(s):  
Mark W. Musch ◽  
Leon Goldstein
Keyword(s):  
Tyrosine Kinase ◽  
Red Blood Cells ◽  
Tyrosine Phosphorylation ◽  
Anion Exchanger ◽  
Blood Cells ◽  
Volume Expansion ◽  
Kinase Inhibitor ◽  
Regulatory Volume Decrease ◽  
Organic Osmolytes

Upon exposure to hypotonic medium, skate red blood cells swell and then reduce their volume by releasing organic osmolytes and associated water. The regulatory volume decrease is inhibited by stilbenes and anion exchange inhibitors, suggesting involvement of the red blood cell anion exchanger skAE1. To determine the role of tyrosine phosphorylation, red blood cells were volume expanded with and without prior treatment with the tyrosine kinase inhibitor piceatannol. At the concentration used, 130 μM, piceatannol nearly completely inhibits p72syk, a tyrosine kinase previously shown to phosphorylate skAE1 (M. W. Musch, E. H. Hubert, and L. Goldstein. J Biol Chem 274: 7923–7928, 1999). Hyposmotic-induced volume expansion stimulated association of p72syk with a light membrane fraction of skate red blood cells. Piceatannol did not inhibit this association but decreased hyposmotically stimulated increased skAE1 tyrosine phophorylation. Movement of skAE1 from an intracellular to a surface detergent-resistant membrane domain and tetramer formation were not inhibited by piceatannol treatment. Two effects of hyposmotic-induced volume expansion, decreased band 4.1 binding and increased ankyrin, were both inhibited by piceatannol. These results suggest that at least one event requiring p72syk activation is pivotal for hyposmotic-induced increased transport; however, steps that do not require tyrosine phosphorylation may also play a role.

The volume-regulated anion channel is formed by LRRC8 heteromers – molecular identification and roles in membrane transport and physiology

2015 ◽  
Vol 396 (9-10) ◽  
pp. 975-990 ◽  
Author(s):  
Tobias Stauber
Keyword(s):  
Cell Biology ◽  
Regulatory Volume Decrease ◽  
Anion Channel ◽  
Cell Swelling ◽  
Transepithelial Transport ◽  
Organic Osmolytes ◽  
Physiological Processes ◽  
Starting Point ◽  
And Migration ◽  
Volume Decrease

Abstract Cellular volume regulation is fundamental for numerous physiological processes. The volume-regulated anion channel, VRAC, plays a crucial role in regulatory volume decrease. This channel, which is ubiquitously expressed in vertebrates, has been vastly characterized by electrophysiological means. It opens upon cell swelling and conducts chloride and arguably organic osmolytes. VRAC has been proposed to be critically involved in various cellular and organismal functions, including cell proliferation and migration, apoptosis, transepithelial transport, swelling-induced exocytosis and intercellular communication. It may also play a role in pathological states like cancer and ischemia. Despite many efforts, the molecular identity of VRAC had remained elusive for decades, until the recent discovery of heteromers of LRRC8A with other LRRC8 family members as an essential VRAC component. This identification marks a starting point for studies on the structure-function relation, for molecular biological investigations of its cell biology and for re-evaluating the physiological roles of VRAC. This review recapitulates the identification of LRRC8 heteromers as VRAC components, depicts the similarities between LRRC8 proteins and pannexins, and discussed whether VRAC conducts larger osmolytes. Furthermore, proposed physiological functions of VRAC and the present knowledge about the physiological significance of LRRC8 proteins are summarized and collated.

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
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