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.

Resistance to osmotic lysis in BXD-31 mouse erythrocytes: association with upregulated K-Cl cotransport

1996 ◽  
Vol 270 (3) ◽  
pp. C866-C877 ◽  
Author(s):  
C. C. Armsby ◽  
A. K. Stuart-Tilley ◽  
S. L. Alper ◽  
C. Brugnara
Keyword(s):  
Normal Cell ◽  
Genetic Locus ◽  
Regulatory Volume Decrease ◽  
Osmotic Fragility ◽  
Cell Swelling ◽  
K Channel ◽  
Cell Dehydration ◽  
Osmotic Lysis ◽  
Volume Decrease ◽  
Characteristic Resistance

The decreased osmotic fragility and reduced K+ content of BXD-31 mouse erythrocytes arise from variation at a single genetic locus. We compared ion transport in erythrocytes from BXD-31 mice and the parental strain, DBA/2J. The strains had similar rates for Na-K pump, Na/H exchange, Na-K-2Cl cotransport, Ca2+ activated K+ channel, or AE1-mediated SO4 transport. In contrast, K-Cl cotransport was twice as active in BXD-31 as in DBA/2J cells. Cl- dependent K+ efflux from BXD-31 cells displayed steep activation by acid pH (with maximal transport occurring at pH 6.75), whereas DBA/2J erythrocytes displayed a far less dramatic response to pH. Both strains displayed regulatory volume decrease in response to cell swelling. However, a 62% greater loss of cell K+ via K-Cl cotransport was observed in the BXD-31 strain. Furthermore the decreased osmotic fragility of BXD-31 red blood cells was normalized by treatment with nystatin to achieve normal cell K+ and water content. Thus upregulated K-Cl cotransport induces cell dehydration and K+ deficit in BXD-31 erythrocytes and causes their characteristic resistance to osmotic lysis.

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 fluxes in vascular endothelial cells: volume regulation via K-Cl cotransport and K channels

1993 ◽  
Vol 265 (3) ◽  
pp. C763-C769 ◽  
Author(s):  
P. B. Perry ◽  
W. C. O'Neill
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
Ionophore A23187 ◽  
Vascular Endothelial ◽  
Aortic Endothelial Cells ◽  
K Channels ◽  
Volume Decrease ◽  
Aortic Endothelial

K efflux pathways responsible for regulatory volume decrease (RVD) were examined in bovine aortic endothelial cells. Hypotonic swelling produced a rapid and reversible threefold increase in bumetanide-insensitive 86Rb efflux. Swelling-activated 86Rb efflux was inhibited 43% when Cl was replaced with NO3, and this Cl-dependent efflux was inhibited by 1 mM furosemide. Neither Cl replacement nor furosemide inhibited the efflux stimulated by a Ca ionophore (A23187) in isotonic medium. Swelling-activated 86Rb efflux was also inhibited by 4,4'-diisothiocyanostilbene-2,2'-disulfonate but not by dinitrostilbenedisulfonate. Cell swelling induced a volume-regulatory K loss that was incomplete in hypotonic medium but complete and more rapid when bumetanide was added or when cells were swollen isosmotically. K loss in the presence of bumetanide was partially blocked by furosemide. We conclude that two separate swelling-activated K fluxes mediate RVD in aortic endothelial cells: a Cl-dependent, furosemide-sensitive, but bumetanide-insensitive flux that is consistent with K-Cl cotransport, and a Cl-independent efflux that presumably is mediated by K channels.

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

TRPM7 Is Involved in Volume Regulation in Salivary Glands

2017 ◽  
Vol 96 (9) ◽  
pp. 1044-1050 ◽  
Author(s):  
J.M. Kim ◽  
S. Choi ◽  
K. Park
Keyword(s):  
Critical Role ◽  
Regulatory Volume Decrease ◽  
Specific Inhibitor ◽  
Acinar Cells ◽  
Cell Swelling ◽  
Hypotonic Solution ◽  
Current Profile ◽  
Patch Clamp Technique ◽  
Extracellular Medium ◽  
Intracellular Ca

Under hypotonic conditions, the regulatory volume decrease (RVD) is essential to maintain physiological homeostasis and functions in diverse biological systems. Intracellular Ca2+ has been reported as an important mediator of this response, but the underlying Ca2+ mechanism responsible for RVD is still controversial. Here we investigate the role of Ca2+ in the RVD response using live-cell imaging, microspectrofluorimetry, and a patch-clamp technique. A typical RVD was observed in submandibular gland acinar cells after swelling in a hypotonic solution, whereas intracellular Ca2+ chelation completely inhibited the RVD response. The incidence and magnitude of the Ca2+ transient were proportional to the degree of hypotonicity of the extracellular medium, and there was a close relationship between intracellular Ca2+ concentration and the volumetric changes of the cells. Notably, this response was mediated by Ca2+-induced Ca2+ release, which is triggered by Ca2+ influx via stretch-activated TRPM7 channels. Furthermore, we detected the generation of Cl− currents in the swelling acinar cells upon hypotonic stress, and the current profile matched that of the Ca2+-activated Cl− currents. A specific inhibitor of Cl− currents also inhibited the RVD response. In conclusion, an intracellular Ca2+ increase in response to osmotically induced cell swelling plays a critical role in RVD in salivary gland acinar cells.

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

Dipyridamole inhibits sickling-induced cation fluxes in sickle red blood cells

Blood ◽  
2001 ◽  
Vol 97 (12) ◽  
pp. 3976-3983 ◽  
Author(s):  
Clinton H. Joiner ◽  
Maorong Jiang ◽  
William J. Claussen ◽  
Nancy J. Roszell ◽  
Zahida Yasin ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
K Channel ◽  
Ionophore A23187 ◽  
Anion Conductance ◽  
Rbc Membrane ◽  
Cellular Dehydration ◽  
Sickle Red Blood Cells

Sickling-induced cation fluxes contribute to cellular dehydration of sickle red blood cells (SS RBCs), which in turn potentiates sickling. This study examined the inhibition by dipyridamole of the sickling-induced fluxes of Na+, K+, and Ca++ in vitro. At 2% hematocrit, 10 μM dipyridamole inhibited 65% of the increase in net fluxes of Na+ and K+ produced by deoxygenation of SS RBCs. Sickle-induced Ca++ influx, assayed as 45Ca++uptake in quin-2–loaded SS RBCs, was also partially blocked by dipyridamole, with a dose response similar to that of Na+and K+ fluxes. In addition, dipyridamole inhibited the Ca++-activated K+ flux (via the Gardos pathway) in SS RBCs, measured as net K+ efflux in oxygenated cells exposed to ionophore A23187 in the presence of external Ca++, but this effect resulted from reduced anion conductance, rather than from a direct effect on the K+channel. The degree of inhibition of sickling-induced fluxes was dependent on hematocrit, and up to 30% of dipyridamole was bound to RBC membranes at 2% hematocrit. RBC membrane content of dipyridamole was measured fluorometrically and correlated with sickling-induced flux inhibition at various concentrations of drug. Membrane drug content in patients taking dipyridamole for other clinical indications was similar to that producing inhibition of sickling-induced fluxes in vitro. These data suggest that dipyridamole might inhibit sickling-induced fluxes of Na+, K+, and Ca++ in vivo and therefore have potential as a pharmacological agent to reduce SS RBC dehydration.

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