Volumetric response of vertebrate hepatocytes challenged by osmotic gradients: A theoretical approach

Espelt, María V.; Alleva, Karina; Amodeo, Gabriela; Krumschnabel, Gerhard; Rossi, R.; Schwarzbaum, Pablo J.

doi:10.1016/j.cbpb.2008.02.001

Cited by 7 publications

(11 citation statements)

References 30 publications

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“…A "symmetrical" type of biophysical model is therefore adequate to simulate the results obtained in our experiments. The model cell was treated as a symmetric entity (apical and basolateral side were not considered separately) bathed with homogenous solution, like in previously reported models (Hernandez and Chifflet 2000;Fraser and Huang 2004;Espelt et al 2008). Thus our experimental design allowed us to use a simple "symmetrical" model to study polarized epithelial cells, which could be viewed as an advantage of the current approach.…”

Section: Discussionmentioning

confidence: 99%

Quantitative estimation of transmembrane ion transport in rat renal collecting duct principal cells

Ilyaskin

Karpov²,

Медведев³

et al. 2014

gpb

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Abstract. Kidney collecting duct principal cells play a key role in regulated tubular reabsorption of water and sodium and secretion of potassium. The importance of this function for the maintenance of the osmotic homeostasis of the whole organism motivates extensive study of the ion transport properties of collecting duct principal cells.We performed experimental measurements of cell volume and intracellular sodium concentration in rat renal collecting duct principal cells from the outer medulla (OMCD) and used a mathematical model describing transmembrane ion fluxes to analyze the experimental data. The sodium and chloride concentrations ([Na + ] in = 37.3 ± 3.3 mM, [Cl -] in = 32.2 ± 4.0 mM) in OMCD cells were quantitatively estimated. Correspondence between the experimentally measured cell physiological characteristics and the values of model permeability parameters was established. Plasma membrane permeabilities and the rates of transmembrane fluxes for sodium, potassium and chloride ions were estimated on the basis of ion substitution experiments and model predictions. In particular, calculated sodium (P Na ), potassium (P K ) and chloride (P Cl ) permeabilities were equal to 3.2 × 10 -6 cm/s, 1.0 × 10 -5 cm/s and 3.0 × 10 -6 cm/s, respectively. This approach sets grounds for utilization of experimental measurements of intracellular sodium concentration and cell volume to quantify the ion permeabilities of OMCD principal cells and aids us in understanding the physiology of the adjustment of renal sodium and potassium excretion.

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Section: Discussionmentioning

confidence: 99%

Quantitative estimation of transmembrane ion transport in rat renal collecting duct principal cells

Ilyaskin

Karpov²,

Медведев³

et al. 2014

gpb

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“…Cell volume regulation mechanisms have been studied in several mammalian cell types, for example, Ehrlich ascites tumor cells (reviewed in [1]), lymphocytes [7], hepatocytes [8], vascular smooth muscle cells [9], renal [10,11], intestinal [12,13] and lens epithelial cells [14]. However, their occurrence in lower Metazoa is still far from being established.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of Hyposmotic Volume Regulation in Isolated Nematocytes of the Anthozoan <i>Aiptasia diaphana</i>

Marino¹,

Morabito²,

Spada³

et al. 2010

Cell Physiol Biochem

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The nature and role of potassium (K) and water transport mediating hyposmotically-induced regulatory volume decrease (RVD) were studied in nematocytes dissociated with 605 mM thiocyanate from acontia of the Anthozoan Aiptasia diaphana. Cell volume and hence RVD were calculated from the inverse ratios of the cross sectional areas of nematocytes (A/A_o) measured before (A_o) and after (A) challenge with 65% artificial sea water (ASW). To distinguish between K channels and K-Cl cotransport (KCC), external sodium (Na) and chloride (Cl) were replaced by K and nitrate (NO₃), respectively. Inhibitors were added to identify K channels (barium, Ba), and putative kinase (N-ethylmaleimide, NEM) and phosphatase (okadaic acid, OA) regulation of KCC. In 65% NaCl ASW, nematocytes displayed a biphasic change in A/A_o, peaking within 4 min due to osmotic water entry and thereafter declining within 6 min due to RVD. Changing NaCl to KCl or NaNO₃ ASW did not affect the osmotic phase but attenuated RVD, consistent with K channel and KCC mechanisms. Ba (3 mM) inhibited RVD. NEM and OA, applied separately, inhibited the osmotic phase and muted RVD suggesting primary action on water transport (aquaporins). NEM and OA together reduced the peak A/A_o ratio during the osmotic phase whereas RVD was inhibited when OA preceded NEM. Thus, both K channels and KCC partake in the nematocyte RVD, the extent of which is determined by functional thiols and dephosphorylation of putative aquaporins facilitating the preceding osmotic water shifts.

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“…Although the ability to regulate cell volume is widespread among cell types and species (Hoffmann et al 2009;Marshall 2010), it is not universal. For example, hypotonic swelling is not followed by a concomitant RVD in goldfish hepatocytes (Espelt et al 2008) and human RBCs do not display volume recovery in response to hypotonic stress (unpublished results). Another major finding of our study is that RVD in salmon RBCs occurred via Fig.…”

Section: Discussionmentioning

confidence: 91%

“…We also considered that this species is optionally anadromous (Hoar 1988) and thus potentially exposed to large fluctuations in external salinity. In addition, despite reports concerning cell volume regulation in several species of fish, including trout (Kanli and Norderhus 1998;Egee et al 2000;Guizouarn et al 2000;Leguen and Prunet 2004;Espelt et al 2008), turbot (Ollivier et al 2006), eel (Lionetto et al 2005;Trischitta et al 2005), catfish (Goswami and Saha 2006), and little skate (Puffer et al 2006), there is a surprising paucity of data regarding RVD in salmon. Accordingly, the purpose of this study was to investigate the cellular basis by which salmon RBCs regulate volume under hypotonic conditions.…”

Section: Introductionmentioning

confidence: 87%

“…from a resting level of approximately 50-100 nM to a stimulated level of 1-10 lM occurs as a rapid response to a number of cellular stimuli, including growth factors, neurotransmitters, hormones, peptides, toxins, and cell swelling (Foskett 1994). Although the cellular mechanisms that activate and regulate permeability pathways during RVD are not completely understood and differ between cell types (Wehner et al 2003;Espelt et al 2008;Hoffmann et al 2009), Ca 2? has been shown to play a key role in a number of cases (Foskett 1994; Pasantes-Morales and Morales 2000; Tinel et al 2000;Leguen and Prunet 2004;Ollivier et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Regulatory volume response following hypotonic stress in Atlantic salmon erythrocytes

Wormser

Mason

Helm

et al. 2011

Fish Physiol Biochem

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The purpose of this study was to examine regulatory volume decrease (RVD) in Atlantic salmon red blood cells (RBCs). Osmotic fragility was determined optically, mean cell volume was measured electronically, and changes in intracellular Ca(2+) concentration were visualized using fluorescence microscopy and fluo-4-AM. Cells displayed an increase in osmotic fragility and an inhibition of volume recovery following hypotonic shock when they were exposed to a high taurine Ringer or when placed in a high K(+) medium. Interestingly, RVD in cells from fish collected during the summer depended more on taurine efflux, whereas fall cells relied more on the loss of K(+). In addition, RVD in fall cells was prevented with the K(+) channel inhibitor quinine, whereas the ionophore gramicidin decreased osmotic fragility and potentiated volume recovery. Further, hypotonic shock (0.5X Ringer) for both summer and fall cells caused an increase in cytosolic Ca(2+), which resulted from influx of this ion because it was not observed when extracellular Ca(2+) was chelated with EGTA (10 nM free Ca(2+)). Cells exposed to a low Ca(2+) hypotonic Ringer also had a greater osmotic fragility and failed to recover from hypotonic swelling. Finally, inhibition of phospholipase A(2) with ONO-RS-082 blocked volume recovery. In conclusion, Atlantic salmon RBCs displayed volume decrease in response to hypotonic shock, which depended on a swelling-induced influx of Ca(2+) and an increase in the efflux of K(+) and taurine.

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Volumetric response of vertebrate hepatocytes challenged by osmotic gradients: A theoretical approach

Cited by 7 publications

References 30 publications

Quantitative estimation of transmembrane ion transport in rat renal collecting duct principal cells

Quantitative estimation of transmembrane ion transport in rat renal collecting duct principal cells

Mechanisms of Hyposmotic Volume Regulation in Isolated Nematocytes of the Anthozoan <i>Aiptasia diaphana</i>

Regulatory volume response following hypotonic stress in Atlantic salmon erythrocytes

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