K+ conductance activated during regulatory volume decrease. The channels in Ehrlich cells and their possible molecular counterpart

2001 ◽  
Vol 130 (3) ◽  
pp. 565-575 ◽  
Author(s):  
M Niemeyer
Keyword(s):  
Regulatory Volume Decrease ◽  
Ehrlich Cells ◽  
Volume Decrease

Activation of Cl-dependent K transport in Ehrlich ascites tumor cells

1986 ◽  
Vol 251 (3) ◽  
pp. C369-C379 ◽  
Author(s):  
B. Kramhoft ◽  
I. H. Lambert ◽  
E. K. Hoffmann ◽  
F. Jorgensen
Keyword(s):  
Regulatory Volume Decrease ◽  
Extracellular Ph ◽  
Cell Swelling ◽  
Disulfonic Acid ◽  
Cell Shrinkage ◽  
Ehrlich Cells ◽  
Ehrlich Ascites ◽  
Dependent Component ◽  
Ca Depletion ◽  
Volume Decrease

N-ethylmaleimide (NEM) treatment of steady-state Ehrlich cells induces a substantial net loss of cellular KCl and cell shrinkage. The majority of the initial K loss is Cl dependent. From estimates of membrane potential it is concluded that the NEM-induced KCl loss is electroneutral. The effect of NEM on H extrusion by cells in 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-containing medium showed that only an insignificant part of the K loss could be attributed to an activation of a K-H exchange system. Consequently, NEM appears to activate a K-Cl cotransport, which causes cell shrinkage. The anion preference of the K loss is Cl greater than Br much greater than SCN = NO3. NEM also seems to inhibit a Cl-dependent Na uptake previously described in shrunken cells. Addition of NEM to cells undergoing regulatory volume decrease after swelling in hyposmotic media results in a Cl-dependent acceleration of cell shrinkage, suggesting that a Cl-dependent component of K efflux is induced by NEM also in swollen cells. A Cl-dependent K efflux is also activated in Ca-depleted cells or at reduced extracellular pH after cell swelling. Under isotonic conditions activation of Cl-dependent K flux after Ca depletion or pH reduction could not be demonstrated. The combined results show that Ehrlich cells possess a latent K-Cl cotransport that becomes active after changes in the state of SH groups, regardless of the initial cell volume. A similar K-Cl cotransport is activated in hypotonically swollen cells after Ca depletion or after reduction of the extracellular pH.

Human Platelets Exposed to Mechanical Stresses Express a Potent Lipoxygenase Product

1992 ◽  
Vol 68 (05) ◽  
pp. 589-594 ◽  
Author(s):  
Alon Margalit ◽  
Avinoam A Livne
Keyword(s):  
Regulatory Volume Decrease ◽  
Human Platelets ◽  
Mechanical Stresses ◽  
Arterial Stenosis ◽  
Platelet Suspension ◽  
Suspension Flows ◽  
Lipoxygenase Product ◽  
Pathological Conditions ◽  
K Permeability ◽  
Volume Decrease

SummaryHuman platelets exposed to hypotonicity undergo regulatory volume decrease (RVD), controlled by a potent, yet labile, lipoxygenase product (LP). LP is synthesized and excreted during RVD affecting selectively K+ permeability. LP is assayed by its capacity to reconstitute RVD when lipoxygenase is blocked. Centrifugation for preparing washed platelets (1,550 × g, 10 min) is sufficient to express LP activity, with declining potency in repeated centrifugations, indicating that it is not readily replenish-able. When platelet suspension flows in a vinyl tubing (1 mm i.d.), at physiological velocity, controlled at 90–254 cm/s, LP formation increases as a function of velocity but declines as result of increasing the tubing length. Stirring the platelets in an aggregometer cuvette for 30 s, yields no LP unless the stirring is intermittent. No associated platelet lysis or aggregation are observed following the mechanical stress applications. These results demonstrate that although mechanical stresses result in LP production, the mode of its application plays a major role. These results may indicate that LP is synthesized under pathological conditions and could be of relevance to platelets behavior related to arterial stenosis.

LRRC8A is essential for swelling‐activated chloride current and for regulatory volume decrease in astrocytes

2018 ◽  
Vol 33 (1) ◽  
pp. 101-113 ◽  
Author(s):  
Francesco Formaggio ◽  
Emanuela Saracino ◽  
Maria Grazia Mola ◽  
Shreyas Balachandra Rao ◽  
Mahmood Amiry-Moghaddam ◽  
...  
Keyword(s):  
Regulatory Volume Decrease ◽  
Chloride Current ◽  
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.

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.

scholarly journals Release of taurine and glutamate contributes to cell volume regulation in human retinal Müller cells: differences in modulation by calcium

2018 ◽  
Vol 120 (3) ◽  
pp. 973-984 ◽  
Author(s):  
Vanina Netti ◽  
Alejandro Pizzoni ◽  
Martha Pérez-Domínguez ◽  
Paula Ford ◽  
Herminia Pasantes-Morales ◽  
...  
Keyword(s):  
Cell Volume ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Müller Cells ◽  
Anion Channel ◽  
Müller Cell ◽  
Regulatory Mechanisms ◽  
Muller Cells ◽  
Muller Cell ◽  
Volume Decrease

Neuronal activity in the retina generates osmotic gradients that lead to Müller cell swelling, followed by a regulatory volume decrease (RVD) response, partially due to the isoosmotic efflux of KCl and water. However, our previous studies in a human Müller cell line (MIO-M1) demonstrated that an important fraction of RVD may also involve the efflux of organic solutes. We also showed that RVD depends on the swelling-induced Ca2+ release from intracellular stores. Here we investigate the contribution of taurine (Tau) and glutamate (Glu), the most relevant amino acids in Müller cells, to RVD through the volume-regulated anion channel (VRAC), as well as their Ca2+ dependency in MIO-M1 cells. Swelling-induced [3H]Tau/[3H]Glu release was assessed by radiotracer assays and cell volume by fluorescence videomicroscopy. Results showed that cells exhibited an osmosensitive efflux of [3H]Tau and [3H]Glu (Tau > Glu) blunted by VRAC inhibitors 4-(2-butyl-6,7-dichloro-2-cyclopentylindan-1-on-5-yl)-oxybutyric acid and carbenoxolone reducing RVD. Only [3H]Tau efflux was mainly dependent on Ca2+ release from intracellular stores. RVD was unaffected in a Ca2+-free medium, probably due to Ca2+-independent Tau and Glu release, but was reduced by chelating intracellular Ca2+. The inhibition of phosphatidylinositol-3-kinase reduced [3H]Glu efflux but also the Ca2+-insensitive [3H]Tau fraction and decreased RVD, providing evidence of the relevance of this Ca2+-independent pathway. We propose that VRAC-mediated Tau and Glu release has a relevant role in RVD in Müller cells. The observed disparities in Ca2+ influence on amino acid release suggest the presence of VRAC isoforms that may differ in substrate selectivity and regulatory mechanisms, with important implications for retinal physiology. NEW & NOTEWORTHY The mechanisms for cell volume regulation in retinal Müller cells are still unknown. We show that swelling-induced taurine and glutamate release mediated by the volume-regulated anion channel (VRAC) largely contributes the to the regulatory volume decrease response in a human Müller cell line. Interestingly, the hypotonic-induced efflux of these amino acids exhibits disparities in Ca2+-dependent and -independent regulatory mechanisms, which strongly suggests that Müller cells may express different VRAC heteromers formed by the recently discovered leucine-rich repeat containing 8 (LRRC8) proteins.

Regulation of cellular volume in rabbit ventricular myocytes: bumetanide, chlorothiazide, and ouabain

1991 ◽  
Vol 260 (1) ◽  
pp. C122-C131 ◽  
Author(s):  
K. Drewnowska ◽  
C. M. Baumgarten
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Ventricular Myocytes ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Volume Response ◽  
Rabbit Ventricular Myocytes ◽  
Cell Volumes ◽  
Measured Volume ◽  
Volume Decrease

Video microscopy was used to study the regulation of cell volume in isolated rabbit ventricular myocytes. Myocytes rapidly (less than or equal to 2 min) swelled and shrank in hyposmotic and hyperosmotic solutions, respectively, and this initial volume response was maintained without a regulatory volume decrease or increase for 20 min. Relative cell volumes (normalized to isosmotic solution, 1T) were as follows: 1.41 +/- 0.01 in 0.6T, 1.20 +/- 0.04 in 0.8T, 0.71 +/- 0.04 in 1.8T, and 0.57 +/- 0.03 in 2.6T. These volume changes were significantly less than expected if all of the measured volume was osmotically active water. Changes in width and thickness were significantly greater than changes in cell length. The idea that cotransport contributes to cell volume regulation was tested by inhibiting Na(+)-K(+)-2Cl- cotransport with bumetanide (BUM) and Na(+)-Cl- cotransport with chlorothiazide (CTZ). Under isotonic conditions, a 10-min exposure to BUM (1 microM), CTZ (100 microM), or BUM (10 microM) plus CTZ (100 microM) decreased relative cell volume to 0.87 +/- 0.01, 0.86 +/- 0.02, and 0.82 +/- 0.04, respectively. BUM plus CTZ also modified the response to osmotic stress. Swelling in 2.6T medium was 76% greater and shrinkage in 0.6T medium was 29% less than in the absence of diuretics. In contrast to the rapid effects of diuretics, inhibition of the Na(+)-K+ pump with 10 microM ouabain for 20 min did not affect cell volume in 1T solution. Nevertheless, ouabain decreased swelling in 0.6T medium by 52% and increased shrinkage in 1.8T medium by 34%. These data suggest that under isotonic conditions Na(+)-K(+)-2Cl- and Na(+)-Cl- cotransport are critical in establishing cell volume, but osmoregulation can compensate for Na(+)-K+ pump inhibition for at least 20 min. Under anisotonic conditions, the Na(+)-K+ pump and Na(+)-K(+)-2Cl- and/or Na(+)-Cl- cotransport are important in myocyte volume regulation.

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