scholarly journals Comparison of Isotonic Activation of Cell Volume Regulation in Rat Peritoneal Mesothelial Cells and in Kidney Outer Medullary Collecting Duct Principal Cells

Biomolecules ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1452
Author(s):  
Galina S. Baturina ◽  
Liubov E. Katkova ◽  
Claus Peter Schmitt ◽  
Evgeniy I. Solenov ◽  
Sotirios G. Zarogiannis
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Cell Volume Regulation ◽  
Mesothelial Cells ◽  
Hypertonic Medium ◽  
Peritoneal Mesothelial Cells ◽  
Principal Cells ◽  
Medullary Collecting Duct

In disease states, mesothelial cells are exposed to variable osmotic conditions, with high osmotic stress exerted by peritoneal dialysis (PD) fluids. They contain unphysiologically high concentrations of glucose and result in major peritoneal membrane transformation and PD function loss. The effects of isotonic entry of urea and myo-inositol in hypertonic (380 mOsm/kg) medium on the cell volume of primary cultures of rat peritoneal mesothelial cells and rat kidney outer medullary collecting duct (OMCD) principal cells were studied. In hypertonic medium, rat peritoneal mesothelial cells activated a different mechanism of cell volume regulation in the presence of isotonic urea (100 mM) in comparison to rat kidney OMCD principal cells. In kidney OMCD cells inflow of urea into the shrunken cell results in restoration of cell volume. In the shrunken peritoneal mesothelial cells, isotonic urea inflow caused a small volume increase and activated regulatory volume decrease (RVD). Isotonic myo-inositol activated RVD in hypertonic medium in both cell types. Isotonic application of both osmolytes caused a sharp increase of intracellular calcium both in peritoneal mesothelial cells and in kidney OMCD principal cells. In conclusion, peritoneal mesothelial cells exhibit RVD mechanisms when challenged with myo-inositol and urea under hyperosmolar isotonic switch from mannitol through involvement of calcium-dependent control. Myo-inositol effects were identical with the ones in OMCD principal cells whereas urea effects in OMCD principal cells led to no RVD induction.

Cell volume regulation of rat kidney collecting duct epithelial cells in hypotonic medium

2011 ◽  
Vol 436 (1) ◽  
pp. 13-15 ◽  
Author(s):  
E. I. Solenov ◽  
G. S. Baturina ◽  
A. V. Ilyaskin ◽  
L. Ye. Katkova ◽  
L. N. Ivanova
Keyword(s):  
Epithelial Cells ◽  
Cell Volume ◽  
Volume Regulation ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Cell Volume Regulation ◽  
Hypotonic Medium ◽  
Kidney Collecting Duct

scholarly journals Role of AQP2 in activation of calcium entry by hypotonicity: implications in cell volume regulation

2008 ◽  
Vol 294 (3) ◽  
pp. F582-F590 ◽  
Author(s):  
L. Galizia ◽  
M. P. Flamenco ◽  
V. Rivarola ◽  
C. Capurro ◽  
P. Ford
Keyword(s):  
Cell Membrane ◽  
Cell Volume ◽  
Volume Regulation ◽  
Collecting Duct ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Calcium Entry ◽  
Cortical Collecting Duct ◽  
Extracellular Medium ◽  
Hypotonic Shock

We previously reported in a rat cortical collecting duct cell line (RCCD1) that the presence of aquaporin 2 (AQP2) in the cell membrane is critical for the rapid activation of regulatory volume decrease mechanisms (RVD) (Ford et al. Biol Cell 97: 687–697, 2005). The aim of our present work was to investigate the signaling pathway that links AQP2 to this rapid RVD activation. Since it has been previously described that hypotonic conditions induce intracellular calcium ([Ca2+]i) increases in different cell types, we tested the hypothesis that AQP2 could have a role in activation of calcium entry by hypotonicity and its implication in cell volume regulation. Using a fluorescent probe technique, we studied [Ca2+]i and cell volume changes in response to a hypotonic shock in WT-RCCD1 (not expressing aquaporins) and in AQP2-RCCD1 (transfected with AQP2) cells. We found that after a hypotonic shock only AQP2-RCCD1 cells exhibit a substantial increase in [Ca2+]i. This [Ca2+]i increase is strongly dependent on extracellular Ca2+ and is partially inhibited by thapsigargin (1 μM) indicating that the rise in [Ca2+]i reflects both influx from the extracellular medium and release from intracellular stores. Exposure of AQP2-RCCD1 cells to 100 μM gadolinium reduced the increase in [Ca2+]i suggesting the involvement of a mechanosensitive calcium channel. Furthermore, exposure of cells to all of the above described conditions impaired rapid RVD. We conclude that the expression of AQP2 in the cell membrane is critical to produce the increase in [Ca2+]i which is necessary to activate RVD in RCCD1 cells.

Role of Na-K-Cl cotransport in vascular endothelial cell volume regulation

1993 ◽  
Vol 264 (5) ◽  
pp. C1316-C1326 ◽  
Author(s):  
M. E. O'Donnell
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Vascular Endothelial ◽  
Cerebral Microvessels ◽  
Hypertonic Medium ◽  
Endothelial Cell Function

Vascular endothelial cells have been shown previously to possess a highly active Na-K-Cl cotransport system that mediates the major portion of total K influx and is regulated by a variety of vasoactive hormones and neurotransmitters. These observations suggest that the cotransporter may be an important component of endothelial cell function. The present study was conducted to investigate the role of Na-K-Cl cotransport in regulation of endothelial cell volume. Cultured bovine aortic endothelial cells were exposed to media of varying tonicities and Na-K-Cl cotransport activity assessed as bumetanide-sensitive K influx. Increasing the extracellular tonicity by increments as small as 10 mosM was found to cause significant stimulation of cotransport activity, and lowering tonicity reduced activity of the transporter. Exposure of endothelial cells to hypertonic medium was also found to increase bumetanide-sensitive net uptake of Na and K and total cellular Na and K content. Endothelial cell volume was evaluated by [14C]urea determination of intracellular water space in endothelial monolayers and by electronic cell sizing of suspended cells. Treatment of the cells with agents that stimulate Na-K-Cl cotransport activity was found to increase cell volume, whereas cotransport-inhibiting agents decreased cell volume. Exposure of the cells to hypertonic medium caused a rapid decrease in cell volume, followed by a regulatory volume increase that was greatly attenuated by bumetanide. The volume recovery was partially inhibited by the Na-H exchange inhibitor amiloride and was nearly abolished by bumetanide and amiloride in combination. Endothelial cells of pulmonary artery and cerebral microvessels were also found to exhibit increased Na-K-Cl cotransport activity on exposure to hypertonic media. These findings suggest that Na-K-Cl cotransport is of major importance in endothelial cell volume regulation.

Immunocytochemical and immunoelectron microscopic localization of α-, β-, and γ-ENaC in rat kidney

2001 ◽  
Vol 280 (6) ◽  
pp. F1093-F1106 ◽  
Author(s):  
Henrik Hager ◽  
Tae-Hwan Kwon ◽  
Anna K. Vinnikova ◽  
Shyama Masilamani ◽  
Heddwen L. Brooks ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Confocal Microscopy ◽  
Subcellular Localization ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Apical Plasma Membrane ◽  
Cortical Collecting Duct ◽  
Principal Cells ◽  
Medullary Collecting Duct ◽  
Epithelial Sodium Channel Enac

Epithelial sodium channel (ENaC) subunit (α, β, and γ) mRNA and protein have been localized to the principal cells of the connecting tubule (CNT), cortical collecting duct (CCD), and outer medullary collecting duct (OMCD) in rat kidney. However, the subcellular localization of ENaC subunits in the principal cells of these cells is undefined. The cellular and subcellular localization of ENaC subunits in rat kidney was therefore examined. Immunocytochemistry demonstrated the presence of all three subunits in principal cells of the CNT, CCD, OMCD, and IMCD. In cortex and outer medulla, confocal microscopy demonstrated a difference in the subcellular localization of subunits. α-ENaC was localized mainly in a zone in the apical domains, whereas β- and γ-ENaC were found throughout the cytoplasm. Immunoelectron microscopy confirmed the presence of ENaC subunits in both the apical plasma membrane and intracellular vesicles. In contrast to the labeling pattern seen in cortex, α-ENaC labeling in IMCD cells was distributed throughout the cytoplasm. In the urothelium covering pelvis, ureters, and bladder, immunoperoxidase and confocal microscopy revealed differences the presence of all ENaC subunits. As seen in CCD, α-ENaC was present in a narrow zone near the apical plasma membrane, whereas β- and γ-ENaC were dispersed throughout the cytoplasm. In conclusion, all three subunits of ENaC are expressed throughout the collecting duct (CD), including the IMCD as well as in the urothelium. The intracellular vesicular pool in CD principal cells suggests ENaC trafficking as a potential mechanism for the regulation of Na+ reabsorption.

Axial heterogeneity in basolateral AQP2 localization in rat kidney: effect of vasopressin

2003 ◽  
Vol 284 (4) ◽  
pp. F701-F717 ◽  
Author(s):  
Birgitte Mønster Christensen ◽  
Weidong Wang ◽  
Jørgen Frøkiær ◽  
Søren Nielsen
Keyword(s):  
Plasma Membrane ◽  
Receptor Antagonist ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Apical Plasma Membrane ◽  
Brattleboro Rats ◽  
Short Term ◽  
Principal Cells ◽  
Medullary Collecting Duct

The purpose of the present study was to examine whether there is axial heterogeneity in the basolateral plasma membrane (BLM) localization of AQP2 and whether altered vasopressin action or medullary tonicity affects the BLM localization of AQP2. Immunocytochemistry and immunoelectron microscopy revealed AQP2 labeling of the BLM in connecting tubule (CNT) cells and inner medullary collecting duct (IMCD) principal cells in normal rats and vasopressin-deficient Brattleboro rats. In contrast there was little basolateral AQP2 labeling in cortical (CCD) and outer medullary collecting duct principal cells. Short-term desamino-Cys1, D-Arg8 vasopressin (dDAVP) treatment (2 h) of Brattleboro rats caused no increase in AQP2 labeling of the BLM. In contrast, long-term dDAVP treatment (6 days) of Brattleboro rats caused an increased BLM labeling in CNT, CCD, and IMCD. Treatment of normal rats with V2-receptor antagonist for 60 min caused retrieval of AQP2 from the apical plasma membrane. Moreover, AQP2 labeling of the BLM was unchanged in CNT and IMCD but increased in CCD. In conclusion, there is an axial heterogeneity in the subcellular localization of AQP2 with prominent AQP2 labeling of the BLM in CNT and IMCD. There was no increase in AQP2 labeling of the BLM in response to short-term dDAVP. Moreover, acute V2-receptor antagonist treatment did not cause retrieval of AQP2 from the BLM. In contrast, long-term dDAVP treatment caused a major increase in AQP2 expression in the BLM in CCD.

Changes in Volume of Peritoneal Mesothelial Cells Exposed to Osmotic Stress

1999 ◽  
Vol 19 (2) ◽  
pp. 119-123 ◽  
Author(s):  
Andrzej Breborowicz ◽  
Alicja Polubinska ◽  
Dimitrios G. Oreopoulos
Keyword(s):  
Cell Volume ◽  
Primary Cultures ◽  
Mesothelial Cell ◽  
Mesothelial Cells ◽  
Regulatory Mechanisms ◽  
Intracellular Uptake ◽  
Glucose Content ◽  
Hypertonic Medium ◽  
Peritoneal Mesothelial Cells ◽  
Cellular Water

Objective To evaluate changes in volume of mesothelial cells exposed to hypertonic medium and the role of volume regulatory mechanisms in adaptation to hyperosmolality. Design Experiments were performed on primary cultures of human peritoneal mesothelial cells. Cell volume was estimated by measuring equilibrated (intracellular/ extracellular space) 14C-urea in cellular water. Cells in monolayers were exposed to hyperosmotic media and changes in cellular water or intracellular uptake of 3H-proline were measured. Results Exposure of mesothelial cell monolayers to hyperosmotic media reduced the cell volume; the effect was proportional to the osmolality of the medium. Volume of cells exposed to medium supplemented with glucose (180 mmol/L) decreased by 26%, p < 0.001, after 30 minutes’ incubation. Prolonged exposure of mesothelial cells to hyperosmotic medium resulted in gradual recovery, after initial decline, of their volume. Intracellular uptake of amino acid 3H-proline increased after 240 minutes’ exposure of the mesothelial cells to medium supplemented with glucose (90 mmol/L) (+40%, p < 0.05). When cells cultured for 7 days in medium supplemented with glucose (45 mmol/L) were exposed to medium with low glucose content (5 mmol/L) their volume increased by 17%, p < 0.05. Conclusion Mesothelial cells shrink after exposure to hypertonic medium. Increased intracellular uptake of amino acids may be one of the regulatory mechanisms that ensure subsequent volume increase in these cells. Mesothelial cells chronically exposed to hypertonic medium swell after transfer to a medium with physiologic osmolality.

scholarly journals Cell Volume and Sodium Content in Rat Kidney Collecting Duct Principal Cells During Hypotonic Shock

2008 ◽  
Vol 2008 ◽  
pp. 1-5 ◽  
Author(s):  
Evgeny I. Solenov
Keyword(s):  
Cell Volume ◽  
Characteristic Time ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Control Level ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Principal Cells ◽  
Hypoosmotic Shock ◽  
Intracellular Sodium Concentration

The purpose of this study was to investigate the time course of the volume-regulatory response and intracellular sodium concentration ([Na+]i) in the principal cells of rat kidney outer medulla collecting duct (OMCD) epithelia during acute swelling in hypotonic medium. Hypotonic shock was created by PBS diluted with 50% of water. Changes in cell volume were measured with calcein quenching method. Intracellular sodium concentration was studied with fluorescence dye Sodium Green. Principal cells of microdissected OMCD fragments swelled very fast. The characteristic time of swelling (τ1) was 0.65±0.05 seconds, and the volume increased more than 60% (92.9±5.6 and 151.3±9.8 μm3 control and peak volumes correspondently, P<.01). After cell volume reached the peak of swelling, the RVD began without lag period. The characteristic time of volume decreasing to new steady-state level (τ2) was 8.9±1.1 seconds. In hypoosmotic medium, cell volume stabilized on higher level in comparison with control (110.3±8.3 μm3, P<.01). After restoration of the medium osmolality to normotonic, cell volume stabilized on significantly low level in comparison with control level (71.4±6.1 μm3, P<.01). During the hypoosmotic shock, [Na+]i decreased from control level in isotonic PBS to the low level in hypoosmotic solution (27.7±1.4 and 5.8±0.23 mM, P<.01). Calculation of sodium content per cell has shown the significant sodium entry into the cells, which caused a temporary increase correlated with the peak of cell volume caused by swelling. The conclusion is made that in our model of hypoosmotic shock, swelling activates transporters with high permeability for Na+ that provides sodium flux into the cells.

scholarly journals Aquaporin-4 Expression in Adult and Developing Mouse and Rat Kidney

2001 ◽  
Vol 12 (9) ◽  
pp. 1795-1804
Author(s):  
YOUNG-HEE KIM ◽  
JAE-HO EARM ◽  
TONGHUI MA ◽  
ALAN S. VERKMAN ◽  
MARK A. KNEPPER ◽  
...  
Keyword(s):  
Proximal Tubule ◽  
Kidney Development ◽  
Collecting Duct ◽  
Rat Kidney ◽  
Aquaporin 4 ◽  
Principal Cells ◽  
Connecting Tubule ◽  
S3 Segment ◽  
Medullary Collecting Duct ◽  
Old Mice

Abstract. Aquaporin-4 (AQP4) is a member of the aquaporin water-channel family. AQP4 is expressed primarily in the brain, but it is also present in the collecting duct of the kidney, where it is located in the basolateral plasma membrane of principal cells and inner medullary collecting duct (IMCD) cells. Recent studies in the mouse also have reported the presence of AQP4 in the basolateral membrane of the proximal tubule. The purpose of this study was to establish the pattern of AQP4 expression during kidney development and in the adult kidney of both the mouse and the rat. Kidneys of adult and 3-, 7-, and 15-d-old mice and rats were preserved for immunohistochemistry and processed using a peroxidase pre-embedding technique. In both the mouse and the rat, strong basolateral immunostaining was observed in IMCD cells and principal cells in the medullary collecting duct at all ages examined. Labeling was weaker in the cortical collecting duct and the connecting tubule, and there was no labeling of connecting tubule cells in the mouse. In adult mouse kidney, strong AQP4 immunoreactivity was observed in the S3 segment of the proximal tubule. However, there was little or no labeling in the cortex or around the corticomedullary junction in 3- and 7-d-old mice. Between 7 and 15 d of age, distinct AQP4 immunoreactivity appeared in the S3 segment of the mouse proximal tubule concomitant with the differentiation of this segment of the nephron. Labeling of proximal tubules was never observed in the rat kidney. These results suggest that there are differences in transepithelial water transport between mouse and rat or that additional, not yet identified water channels exist in the rat proximal tubule.

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