Comparison of cation transport and regulatory volume decrease between red blood cells from the japanese black bear and the dog

2003 ◽  
Vol 12 (1) ◽  
pp. 33-39 ◽  
Author(s):  
H. Fujise ◽  
T. Nakayama ◽  
N. Iwase ◽  
T. Tsubota ◽  
T. Komatsu
1997 ◽  
Vol 273 (3) ◽  
pp. R991-R998 ◽  
Author(s):  
H. Fujise ◽  
K. Abe ◽  
M. Kamimura ◽  
H. Ochiai

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.


2006 ◽  
Vol 16 (1) ◽  
pp. 61-63
Author(s):  
H. Ochiai ◽  
N. Hishiyama ◽  
K. Higa ◽  
K. Koyama ◽  
M. Seita ◽  
...  

1996 ◽  
Vol 270 (4) ◽  
pp. R801-R810
Author(s):  
L. J. Bergeron ◽  
A. J. Stever ◽  
D. B. Light

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.


1995 ◽  
Vol 198 (1) ◽  
pp. 155-165 ◽  
Author(s):  
F Jensen

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.


Author(s):  
Aleksandra Y. Andreyeva ◽  
Elizaveta A. Skverchinskaya ◽  
Stepan Gambaryan ◽  
Aleksander A. Soldatov ◽  
Igor V. Mindukshev

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

2001 ◽  
Vol 281 (6) ◽  
pp. C2003-C2009 ◽  
Author(s):  
Hiroshi Fujise ◽  
Kazunari Higa ◽  
Tomomi Kanemaru ◽  
Miwa Fukuda ◽  
Norma C. Adragna ◽  
...  

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.


1977 ◽  
Vol 69 (5) ◽  
pp. 537-552 ◽  
Author(s):  
PM Cala

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.


1990 ◽  
Vol 258 (6) ◽  
pp. C1169-C1172 ◽  
Author(s):  
J. A. Halperin ◽  
C. Brugnara ◽  
T. Van Ha ◽  
D. C. Tosteson

We have recently reported that voltage-activated fluxes of Na, K, and Ca occur in human red blood cells [J.A. Halperin, C. Brugnara, M. Tosteson, T. Van Ha, and D. C. Tosteson. Am. J. Physiol. 257 (Cell Physiol. 26): C986-C996, 1989]. The cation permeability increases progressively as the membrane potential becomes more inside positive above +20 mV. In this paper we show that this effect also occurs in high-potassium (HK), but not in low-potassium (LK), sheep and dog red blood cells. This result suggests that the voltage-activated cation transport pathway is not the result of nonspecific dielectric breakdown of the lipid bilayer but, rather, relates to some membrane component, presumably a protein, that is expressed in HK human and sheep but not in LK sheep and dog red blood cells.


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