Characterization of the Increase in [Ca2+] i During Hypotonic Shock and the Involvement of Ca2+-activated K+ Channels in the Regulatory Volume Decrease in Human Osteoblast-like Cells

2000 ◽  
Vol 178 (1) ◽  
pp. 11-20 ◽  
Author(s):  
M. Weskamp ◽  
W. Seidl ◽  
S. Grissmer
Keyword(s):  
Regulatory Volume Decrease ◽  
Human Osteoblast ◽  
Hypotonic Shock ◽  
K Channels ◽  
Volume Decrease

Extracellular pH alkalinization by Cl−/HCO3− exchanger is crucial for TASK2 activation by hypotonic shock in proximal cell lines from mouse kidney

2007 ◽  
Vol 292 (2) ◽  
pp. F628-F638 ◽  
Author(s):  
S. L'Hoste ◽  
H. Barriere ◽  
R. Belfodil ◽  
I. Rubera ◽  
C. Duranton ◽  
...  
Keyword(s):  
Cell Lines ◽  
Regulatory Volume Decrease ◽  
Inhibitory Effect ◽  
Buffering Capacity ◽  
Mouse Kidney ◽  
Wild Type ◽  
Cytosolic Ph ◽  
Hypotonic Shock ◽  
External Ph ◽  
Volume Decrease

We have previously shown that K+-selective TASK2 channels and swelling-activated Cl− currents are involved in a regulatory volume decrease (RVD; Barriere H, Belfodil R, Rubera I, Tauc M, Lesage F, Poujeol C, Guy N, Barhanin J, Poujeol P. J Gen Physiol 122: 177–190, 2003; Belfodil R, Barriere H, Rubera I, Tauc M, Poujeol C, Bidet M, Poujeol P. Am J Physiol Renal Physiol 284: F812–F828, 2003). The aim of this study was to determine the mechanism responsible for the activation of TASK2 channels during RVD in proximal cell lines from mouse kidney. For this purpose, the patch-clamp whole-cell technique was used to test the effect of pH and the buffering capacity of external bath on Cl− and K+ currents during hypotonic shock. In the presence of a high buffer concentration (30 mM HEPES), the cells did not undergo RVD and did not develop outward K+ currents (TASK2). Interestingly, the hypotonic shock reduced the cytosolic pH (pHi) and increased the external pH (pHe) in wild-type but not in cftr −/− cells. The inhibitory effect of DIDS suggests that the acidification of pHi and the alkalinization of pHe induced by hypotonicity in wild-type cells could be due to an exit of HCO3−. In conclusion, these results indicate that Cl− influx will be the driving force for HCO3− exit through the activation of the Cl−/HCO3− exchanger. This efflux of HCO3− then alkalinizes pHe, which in turn activates TASK2 channels.

Volume regulation initiated by Na(+)-nutrient cotransport in isolated mammalian villus enterocytes

1991 ◽  
Vol 260 (1) ◽  
pp. G26-G33 ◽  
Author(s):  
R. J. MacLeod ◽  
J. R. Hamilton
Keyword(s):  
Guinea Pig ◽  
Volume Regulation ◽  
Brush Border Membrane ◽  
Regulatory Volume Decrease ◽  
Membrane Vesicles ◽  
Relative Volume ◽  
Cell Shrinkage ◽  
K Channels ◽  
Volume Decrease ◽  
Pig Jejunum

We assessed ion transport during regulatory volume decrease (RVD) in jejunal villus enterocytes, isolated in suspension from guinea pig jejunum and swollen by exposure to L-alanine (L-Ala) or D-glucose (D-Glc) in the presence of Na+. Cell volume was measured electronically. Relative volume of cells (rel vol: cell vol/isotonic vol) within 1 min of L-Ala (20 mM) addition increased (1.10 +/- 0.03, P less than 0.005), but by 5 min there was no difference between cells in L-Ala or 20 mM D-Ala (0.95 +/- 0.02). Cell shrinkage after maximal swelling was greater with L-Ala than with D-Ala (14 +/- 4 vs. 2 +/- 1%, P less than 0.01). Initial swelling generated by L-Ala required extracellular Na+ (P less than 0.02). Volume increased 30 s after D-Glc (20 mM), and cells were larger than cells treated with L-Glc (1.04 +/- 0.01 vs. 0.95 +/- 0.01, P less than 0.001); subsequent cell shrinkage was complete in 2 min (8 +/- 2%, P less than 0.05). Swelling generated by methyl alpha-D-glucoside was prevented by 0.1 mM phloridzin (P less than 0.05). RVD after D-Glc swelling was prevented by inhibitors of K+ channels, 5 mM Ba2+ (P less than 0.001), 100 microM quinine (P less than 0.005), or 25 mM TEA (P less than 0.02), but the same inhibitors completely prevented L-Ala swelling. All inhibitors had no effect on L-Ala uptake into brush-border membrane vesicles in presence of Na+ gradient.(ABSTRACT TRUNCATED AT 250 WORDS)

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 stimulates bile flow, bile acid excretion, and exocytosis in isolated perfused rat liver

1992 ◽  
Vol 262 (5) ◽  
pp. G806-G812 ◽  
Author(s):  
R. Bruck ◽  
P. Haddad ◽  
J. Graf ◽  
J. L. Boyer
Keyword(s):  
Bile Acid ◽  
Bile Flow ◽  
Sodium Taurocholate ◽  
Regulatory Volume Decrease ◽  
Acid Excretion ◽  
K Channels ◽  
Hypotonic Stress ◽  
Bile Acid Excretion ◽  
Second Peak ◽  
Volume Decrease

To study the effect of volume regulation on bile secretory function, isolated perfused rat livers (IPRL) were exposed to hypotonic stress (45 mM NaCl) while bile flow and the biliary excretion of bile acids and horseradish peroxidase (HRP) were assessed. Hypotonic stress induced a biphasic increase in bile flow, which rose in the first minute from 1.1 +/- 0.2 to 1.7 +/- 0.1 microliter.min-1.g liver-1 (P less than 0.01), an effect attributed to rapid osmotic equilibration of water, then increased further between 3 and 5 min to 1.6 +/- 0.1 microliter.min-1.g liver-1 (P less than 0.01, followed by a subsequent return to baseline. HRP excretion in bile increased during the second peak of bile flow from 0.9 +/- 0.2 to 1.1 +/- 0.2 ng.min-1.g liver-1, P less than 0.01. Pretreatment with colchicine but not lumicolchicine completely abolished the latter increase in bile flow and HRP excretion as did BaCl2 (1 mM), an inhibitor of both K+ channels and regulatory volume decrease (RVD) in hepatocytes. When sodium taurocholate was infused (1 mumol/min), hypotonic stress induced an even larger increase in the second peak of bile flow (5.1 +/- 0.7 microliters/g liver, P less than 0.01) and higher rates of bile acid excretion than in control perfusions with bile acid (126.2 +/- 21.0 vs. 99.0 +/- 17.1 nmol.min-1.g liver-1, P less than 0.05). These data suggest that both bile flow and bile acid excretion are stimulated during RVD by mechanisms that involve both K+ channels and microtubule-dependent exocytosis at the canalicular (apical) membrane domain.

Cell volume regulation by the mouse zygote: mechanism of recovery from a volume increase

1997 ◽  
Vol 272 (6) ◽  
pp. C1854-C1861 ◽  
Author(s):  
D. G. Seguin ◽  
J. M. Baltz
Keyword(s):  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Channel Blockers ◽  
Volume Increase ◽  
K Channels ◽  
Cl Channel ◽  
Cl Channels ◽  
Mouse Zygotes ◽  
Volume Decrease

Mouse zygotes regulate their volumes after cell swelling. This regulatory volume decrease (RVD) is rapid and complete. RVD in zygotes was inhibited by K+ or Cl- channel blockers, indicating the participation of such channels in volume recovery. The channels are separate entities, as indicated by the ability of the cation ionophore gramicidin to restore RVD when K+ channels are blocked but not when Cl- channels are blocked. Intracellular Ca2+ concentration increased with cell swelling. Nevertheless, RVD occurred normally in zygotes loaded with the Ca2+ chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, which prevented Ca2+ from increasing above its normal resting concentration. Thus an increase in intracellular Ca2+ is not necessary for zygote RVD; consistent with this, inhibitors of Ca(2+)-activated K+ channels had little or no effect on RVD. RVD in zygotes was also completely inhibited by millimolar amounts of extracellular ATP. ATP has been shown to inhibit current passed by the volume-sensitive organic osmolyte-Cl- channel in other cells, and thus zygotes may have such a channel participating in RVD.

Volume regulation by human lymphocytes: Characterization of the ionic basis for regulatory volume decrease

1982 ◽  
Vol 112 (2) ◽  
pp. 189-196 ◽  
Author(s):  
Roy K. Cheung ◽  
Sergio Grinstein ◽  
Hans-Michael Dosch ◽  
Erwin W. Gelfand
Keyword(s):  
Volume Regulation ◽  
Human Lymphocytes ◽  
Regulatory Volume Decrease ◽  
Ionic Basis ◽  
Volume Decrease
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