Ca2+-activated K+ channels are involved in regulatory volume decrease in acinar cells isolated from the rat lacrimal gland

1994 ◽  
Vol 141 (2) ◽  
Author(s):  
K.-P. Park ◽  
J.S. Beck ◽  
I.J. Douglas ◽  
P.D. Brown
Keyword(s):  
Lacrimal Gland ◽  
Regulatory Volume Decrease ◽  
Acinar Cells ◽  
K Channels ◽  
Volume Decrease

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.

Potentiation of regulatory volume decrease by P2U purinoceptors in HSG-PA cells

1996 ◽  
Vol 270 (1) ◽  
pp. C86-C97 ◽  
Author(s):  
H. D. Kim ◽  
J. W. Bowen ◽  
M. R. James-Kracke ◽  
L. A. Landon ◽  
J. M. Camden ◽  
...  
Keyword(s):  
Salivary Gland ◽  
Driving Force ◽  
Regulatory Volume Decrease ◽  
Cell Swelling ◽  
K Channels ◽  
Anion Conductance ◽  
Medium Osmolarity ◽  
Gland Duct ◽  
Underlying Mechanisms ◽  
Volume Decrease

HSG-PA human salivary gland duct cells exhibit progressively increased regulatory volume decrease (RVD) in response to decreased medium osmolarity. The P2U purinoceptor agonist UTP causes a potentiation of RVD, the extent of which is most pronounced in 220 mosM medium and is least apparent in 180 mosM medium. We examined the underlying mechanisms for this effect. Exposure of HSG-PA cells to UTP promotes Ca2+ mobilization, hyperpolarization, and net K+ efflux, suggesting the participation of Ca(2+)-activated K+ channels in RVD. To delineate the anion counterpart of K+ movement during RVD, cell swelling in the presence of gramicidin, which abolishes the membrane potential, was measured. In response to a sudden dilution in hypotonic media, gramicidin-treated cells swelled immediately, followed by a "secondary swelling" in 180 but not in 220 mosM medium. The results suggest that in 180 mosM cells perform spontaneous RVD mediated by increased anion conductance. In 220 mosM medium in which RVD is minimal, the increase in anion conductance is marginal. In our model of RVD in which cells were challenged by UTP, the ensuing hyperpolarization provides the driving force for net Cl- efflux, which is confirmed by tracer flux studies during purinoceptor-activated RVD. Thus RVD, which has long been regarded as a self-sufficient cellular program, appears to be subject to extracellular control in HSG-PA cells through receptor-mediated processes.

Effects of hyposmotic shock on ion fluxes in isolated trout hepatocytes

1988 ◽  
Vol 137 (1) ◽  
pp. 303-318 ◽  
Author(s):  
L. Bianchini ◽  
B. Fossat ◽  
J. Porthe-Nibelle ◽  
J. C. Ellory ◽  
B. Lahlou
Keyword(s):  
Membrane Permeability ◽  
Cell Volume ◽  
Time Course ◽  
Control Volume ◽  
Regulatory Volume Decrease ◽  
Ion Fluxes ◽  
K Uptake ◽  
K Channels ◽  
Potassium Permeability ◽  
Volume Decrease

Isolated trout hepatocytes exposed to hypotonic Hank's medium (isotonicity × 0.70) swelled to 1.17 times the control volume after 3 min; by 15 min the cell volume had returned to normal. The ouabain-insensitive K+ uptake increased, indicating an immediate rise in K+ membrane permeability. As indicated by analysis of cellular contents, the regulatory volume decrease (RVD) was ensured by a release of intracellular K+. Na+ was not implicated in this mechanism. This potassium permeability induced by hypotonic shock was transient (maximum at 6 min), insensitive to blocking agents of voltage- and Ca2+-dependent K+ channels, and chloride-dependent. This result, together with a time-course of Cl- uptake similar to that of K+, suggests a K+/Cl- cotransport mechanism. This cotransport is inhibited by high furosemide concentrations (10(−3) mol l-1) but not by bumetanide (10(−4) mol l-1) or piretanide (10(−4) mol l-1).

Role of intracellular calcium in volume regulation by rabbit medullary thick ascending limb cells

1991 ◽  
Vol 260 (3) ◽  
pp. F402-F409 ◽  
Author(s):  
C. Montrose-Rafizadeh ◽  
W. B. Guggino
Keyword(s):  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Thick Ascending Limb ◽  
Tetraacetic Acid ◽  
Extracellular Medium ◽  
K Channels ◽  
Luminal Membrane ◽  
Medullary Thick Ascending Limb ◽  
Volume Decrease

Previous studies demonstrated that Ca2(+)-activated K+ channels in luminal membrane of rabbit medullary thick ascending limb cells (MTAL) are activated on exposure of the cells to hyposmotic solutions [J. Taniguchi and W. B. Guggino. Am. J. Physiol. 257 (Renal Fluid Electrolyte Physiol. 26): F347-F352, 1989]. In this study, we investigated the mechanism of activation of Ca2(+)-activated K+ channels in MTAL cells exposed to hyposmotic solutions. MTAL cells swell in hyposmotic medium and regulate volume back toward the starting volume. This regulatory volume decrease (RVD) is inhibited at high medium K+ concentrations or by presence of quinine or Ba2+ in extracellular medium, suggesting involvement of K+ channels. Measurements of intracellular Ca2+ concentrations with fura-2 show that intracellular Ca2+ rises in hyposmotic solutions and that this rise does not occur in absence of extracellular Ca2+. Nifedipine and verapamil also inhibit rise in intracellular Ca2+. Decreasing intracellular Ca2+ by removal of external Ca2+ in presence of EDTA or by chelation of intracellular Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) inhibits RVD. We conclude that hypotonic solutions activate K+ efflux probably via K+ channels and Ca2+ influx via a nifedipine- and verapamil-sensitive pathway. Lowering intracellular Ca2+ removes the ability of MTAL cells to regulate volume in hyposmotic solutions.

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