ArticleJournal of biophysics (Hindawi Publishing Corporation : Online)2008
Cell volume and sodium content in rat kidney collecting duct principal cells during hypotonic shock.
Article in Journal of biophysics (Hindawi Publishing Corporation : Online), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- Unscheduled mInternational journal of molecular sciences · 2025Article
- Structure and mechanism of a tripartite ATP-independent periplasmic TRAP transporter.Nature communications · 2023Article
- A long isoform of the epithelial sodium channel alpha subunit forms a highly active channel.Channels (Austin, Tex.) · 2015Article
- The influence of increased NaCl uptake on the transport of Na+ and K+ across the plasma membrane of rat renal collecting duct principal cells.Doklady. Biochemistry and biophysics · 2013Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (tau(1)) was 0.65 +/- 0.05 seconds, and the volume increased more than 60% (92.9 +/- 5.6 and 151.3 +/- 9.8 microm(3) 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 (tau(2)) was 8.9 +/- 1.1 seconds. In hypoosmotic medium, cell volume stabilized on higher level in comparison with control (110.3 +/- 8.3 microm(3), 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 microm(3), 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.
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Registered trials
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