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.

scholarly journals Human trabecular meshwork cell volume regulation

2002 ◽  
Vol 283 (1) ◽  
pp. C315-C326 ◽  
Author(s):  
Claire H. Mitchell ◽  
Johannes C. Fleischhauer ◽  
W. Daniel Stamer ◽  
K. Peterson-Yantorno ◽  
Mortimer M. Civan
Keyword(s):  
Cell Volume ◽  
Trabecular Meshwork ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Channel Blockers ◽  
Uptake Mechanism ◽  
Fluid Uptake ◽  
Intracellular Ca ◽  
Predominant Effect ◽  
Volume Decrease

The volume of certain subpopulations of trabecular meshwork (TM) cells may modify outflow resistance of aqueous humor, thereby altering intraocular pressure. This study examines the contribution that Na+/H+, Cl−/HCO[Formula: see text]exchange, and K+-Cl− efflux mechanisms have on the volume of TM cells. Volume, Cl− currents, and intracellular Ca2+ activity of cultured human TM cells were studied with calcein fluorescence, whole cell patch clamping, and fura 2 fluorescence, respectively. At physiological bicarbonate concentration, the selective Na+/H+ antiport inhibitor dimethylamiloride reduced isotonic cell volume. Hypotonicity triggered a regulatory volume decrease (RVD), which could be inhibited by the Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), the K+channel blockers Ba2+ and tetraethylammonium, and the K+-Cl− symport blocker [(dihydroindenyl)oxy]alkanoic acid. The fluid uptake mechanism in isotonic conditions was dependent on bicarbonate; at physiological levels, the Na+/H+ exchange inhibitor dimethylamiloride reduced cell volume, whereas at low levels the Na+-K+-2Cl− symport inhibitor bumetanide had the predominant effect. Patch-clamp measurements showed that hypotonicity activated an outwardly rectifying, NPPB-sensitive Cl− channel displaying the permeability ranking Cl− > methylsulfonate > aspartate. 2,3-Butanedione 2-monoxime antagonized actomyosin activity and both increased baseline [Ca2+] and abolished swelling-activated increase in [Ca2+], but it did not affect RVD. Results indicate that human TM cells display a Ca2+-independent RVD and that volume is regulated by swelling-activated K+ and Cl− channels, Na+/H+ antiports, and possibly K+-Cl− symports in addition to Na+-K+-2Cl− symports.

Dihydropyridine-sensitive cell volume regulation in proximal tubule: the calcium window

1990 ◽  
Vol 259 (6) ◽  
pp. F950-F960 ◽  
Author(s):  
N. A. McCarty ◽  
R. G. O'Neil
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Channel Blockers ◽  
Ca Channel ◽  
Hypotonic Solution ◽  
Dependent Manner ◽  
Intracellular Ca

The mechanism underlying the activation of hypotonic cell volume regulation was studied in rabbit proximal straight tubule (PST). When isolated non-perfused tubules were exposed to hypotonic solution, cells swelled rapidly and then underwent a regulatory volume decrease (RVD). The extent of regulation after swelling was highly dependent on extracellular Ca concentration ([Ca2+]o), with a half-maximal inhibition (K1/2) for [Ca2+]o of approximately 100 microM. RVD was blocked by the Ca-channel blockers verapamil, lanthanum, and the dihydropyridines (DHP) nifedipine and nitrendipine, implicating voltage-activated Ca channels in the RVD response. Using the fura-2 fluorescence-ratio technique, we observed that cell swelling caused a sustained rise in intracellular Ca ([Ca2+]i) only when [Ca2+]o was normal (1 mM) but not when [Ca2+]o was low (1-10 microM). Furthermore, external Ca was required early on during swelling to induce RVD. If RVD was initially blocked by reducing [Ca2+]o or by addition of verapamil during hypotonic swelling, volume regulation could only be restored by subsequently inducing Ca entry within the first 1 min or less of exposure to hypotonic solution. These data indicate a "calcium window" of less than 1 min, during which RVD is sensitive to Ca, and that part of the Ca-dependent mechanism responsible for achieving RVD undergoes inactivation after swelling. It is concluded that RVD in rabbit PST is modulated by Ca via a DHP-sensitive mechanism in a time-dependent manner.

Hyposmotic activation of ICl,swell in rabbit nonpigmented ciliary epithelial cells involves increased ClC-3 trafficking to the plasma membrane

2004 ◽  
Vol 82 (6) ◽  
pp. 708-718 ◽  
Author(s):  
John P Vessey ◽  
Chanjuan Shi ◽  
Christine AB Jollimore ◽  
Kelly T Stevens ◽  
Miguel Coca-Prados ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Membrane Trafficking ◽  
Kinase Inhibitor ◽  
Regulatory Volume Decrease ◽  
Membrane Dynamics ◽  
Cell Swelling ◽  
Cl Channels ◽  
Phosphoinositide 3 Kinase ◽  
Nonpigmented Ciliary Epithelial ◽  
Volume Decrease

In mammalian nonpigmented ciliary epithelial (NPE) cells, hyposmotic stimulation leading to cell swelling activates an outwardly rectifying Cl– conductance (ICl,swell), which, in turn, results in regulatory volume decrease. The aim of this study was to determine whether increased trafficking of intracellular ClC-3 Cl channels to the plasma membrane could contribute to the ICl,swell following hyposmotic stimulation. Our results demonstrate that hyposmotic stimulation reversibly activates an outwardly rectifying Cl– current that is inhibited by phorbol-12-dibutyrate and niflumic acid. Transfection with ClC-3 antisense, but not sense, oligonucleotides reduced ClC-3 expression as well as ICl,swell. Intracellular dialysis with 2 different ClC-3 antibodies abolished activation of ICl,swell. Immunofluorescence microscopy showed that hyposmotic stimulation increased ClC-3 immunoreactivity at the plasma membrane. To determine whether this increased expression of ClC-3 at the plasma membrane could be due to increased vesicular trafficking, we examined membrane dynamics with the fluorescent membrane dye FM1-43. Hyposmotic stimulation rapidly increased the rate of exocytosis, which, along with ICl,swell, was inhibited by the phosphoinositide-3-kinase inhibitor wortmannin and the microtubule disrupting agent, nocodazole. These findings suggest that ClC-3 channels contribute to ICl,swell following hyposmotic stimulation through increased trafficking of channels to the plasma membrane.Key words: ClC-3, NPE, cell swelling, membrane trafficking, ciliary body epithelium.

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.

Effects of arginine vasopressin on cell volume regulation in brain astrocyte in culture

1999 ◽  
Vol 276 (3) ◽  
pp. E596-E601 ◽  
Author(s):  
Darya Sarfaraz ◽  
Cosmo L. Fraser
Keyword(s):  
Cell Volume ◽  
Arginine Vasopressin ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Hypotonic Medium ◽  
Receptor Antagonists ◽  
Volume Increase ◽  
Glucose Water ◽  
Water Space ◽  
Volume Decrease

Astrocytes initially swell when exposed to hypotonic medium but rapidly return to normal volume by the process of regulatory volume decrease (RVD). The role that arginine vasopressin (AVP) plays in hypotonically mediated RVD in astrocytes is unknown. This study was therefore designed to determine whether AVP might play a role in astrocyte RVD. With the use of 3- O-[3H]methyl-d-glucose to determine water space, AVP treatment resulted in significantly increased 3- O-methyl-d-glucose water space within 30 s of hypotonic exposure ( P = 0.0001) and remained significantly elevated above baseline (1.75 μl/mg protein) at 5 min ( P < 0.021). In contrast, in untreated cells, complete RVD was achieved by 5 min. At 30 s, cell volume with AVP treatment was 37% greater than in cells that received no treatment (2.9 vs. 2.26 μl/mg protein, respectively; P < 0.006). The rate of cell volume increase (dV/d t) over 30 s was highly significant (0.038 vs. 0.019 μl ⋅ mg protein−1 ⋅ s−1in the AVP-treated vs. untreated group; P = 0.0004 by regression analysis). Additionally, the rate of cell volume decrease over the next 4.5 min was also significantly greater with vasopressin treatment (−dV/d t = 0.0027 vs. 0.0013 μl ⋅ mg protein−1 ⋅ s−1; P = 0.0306). The effect of AVP was concentration dependent with EC50= 3.5 nM. To determine whether AVP action was receptor mediated, we performed RVD studies in the presence of the V1-receptor antagonists benzamil and ethylisopropryl amiloride and the V2-receptor agonist 1-desamino-8-d-arginine vasopressin (DDAVP). Both V1-receptor antagonists significantly inhibited AVP-mediated volume increase by 40–47% ( P < 0.005), whereas DDAVP had no stimulatory effects above control. Taken together, these data suggest that AVP treatment of brain astrocytes in culture appears to increase 3- O-methyl-d-glucose water space during RVD through V1receptor-mediated mechanisms. The significance of these findings is presently unclear.

scholarly journals Cell Volume Regulation in the Epidermis

2021 ◽  
Vol 55 (S1) ◽  
pp. 57-70
Keyword(s):  
Cell Volume ◽  
Current Knowledge ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Skin Layer ◽  
Cell Swelling ◽  
Volume Changes ◽  
Barrier Formation ◽  
Molecular Machinery ◽  
Volume Decrease

In order to cope with external stressors such as changes in humidity and temperature or irritating substances, the epidermis as the outermost skin layer forms a continuously renewing and ideally intact protective barrier. Under certain circumstances, this barrier can be impaired and epidermal cells have to counteract cell swelling or shrinkage induced by osmotic stress via regulatory volume decrease (RVD) or increase (RVI). Here, we will review the current knowledge regarding the molecular machinery underlying RVD and RVI in the epidermis. Furthermore, we will discuss the current understanding how cell volume changes and its regulators are associated with epidermal renewal and barrier formation.

Ion concentration changes in renal cells during regulatory volume decrease

1993 ◽  
Vol 265 (1) ◽  
pp. F77-F86 ◽  
Author(s):  
R. Rick
Keyword(s):  
Collecting Duct ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Zealand White Rabbit ◽  
Ion Concentration ◽  
Cell Swelling ◽  
Minor Role ◽  
Thick Ascending Limb ◽  
Concentration Changes ◽  
Volume Decrease

Electron-probe microanalysis was employed to follow ion concentration changes during regulatory volume decrease. The measurements were performed on isolated tubule bundles, which were dissected from medullary rays of New Zealand White rabbit kidneys. Cell swelling and subsequent regulatory volume decrease were induced by incubating the bundles in 190 mosM medium; control bundles were incubated in 290 mosM medium. Under both conditions, the detectable ions accounted for approximately 80% of the intracellular osmolarity. All cells lost significant amounts of Na, K, and Cl during cell volume regulation. While in the proximal straight tubule more than one-half of the ions lost were Na and Cl, in principal and intercalated cells of the cortical collecting duct and in the thick ascending limb the losses of Na and Cl played only a minor role. The efflux of Na and K greatly exceeded the Cl efflux, suggesting the loss of an additional undetectable anion (bicarbonate). Separate measurements in the nucleus, cytoplasm, and several cellular organelles revealed some inhomogeneity of the subcellular ion distribution.

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.

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.

Volume-activated calcium uptake: its role in cell volume regulation of Madin-Darby canine kidney cells

1992 ◽  
Vol 262 (2) ◽  
pp. C339-C347 ◽  
Author(s):  
A. Rothstein ◽  
E. Mack
Keyword(s):  
Mdck Cells ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Madin Darby Canine Kidney ◽  
Sequence Of Events ◽  
Osmotic Water ◽  
Cl Channels ◽  
Darby Canine Kidney ◽  
Canine Kidney

Immediately after osmotic swelling of Madin-Darby canine kidney (MDCK) cells, a transient (1-2 min) increase in Ca2+ influx and internal Ca2+ (Ca2+i) is observed. The normal Ca2+ influx appears to be mediated by the 3Na(+)-Ca2+ exchange system [Borle et al. Am. J. Physiol. 259 (Cell Physiol. 28): C19-C25, 1990], but the swelling-induced component is different in 1) Na+ dependence, 2) affinity for Ca2+, 3) inhibition by La3+, and 4) direction of net flux at low external Ca2+. Swelling appears to activate an uncoupled Ca2+ flow, perhaps through cation-nonspecific stretch-activated channels. The regulatory volume decrease (RVD) is dependent on the swelling-induced pulse of Ca2+ influx and associated rise in Ca2+i. Swelling also induces a biphasic change in membrane potential, a hyperpolarization followed by depolarization, reflecting sequential increases in K+ and Cl- permeabilities. The time dependence of the former corresponds closely with the transient peak in Ca2+i, but the latter does not. Ca2+i appears to have a direct activating effect on K+ channels but an indirect effect on Cl- channels, mediated via other Ca(2+)-triggered systems. The sequence of events following cell swelling appears to be transient increases in Ca2+ permeability, Ca2+ influx, Ca2+i, K+ permeability, followed by triggering of a mediating system that increases Cl- permeability. The net result is KCl, osmotic water loss, and volume adjustment.

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