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Volume-sensitive K influx in human red cell ghosts
K influx into resealed human red cell ghosts increases when the ghosts are swollen. The influx demonstrates properties similar to volume- sensitive K fluxes present in other cells. The influx is, for the most part, insensitive to the nature of the major intracellular cation and therefore is not a K-...
Formato: | Texto |
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Lenguaje: | English |
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The Rockefeller University Press
1988
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2228920/ https://www.ncbi.nlm.nih.gov/pubmed/2853201 |
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collection | PubMed |
description | K influx into resealed human red cell ghosts increases when the ghosts are swollen. The influx demonstrates properties similar to volume- sensitive K fluxes present in other cells. The influx is, for the most part, insensitive to the nature of the major intracellular cation and therefore is not a K-K exchange. The influx is much greater when the major anion is Cl than when the major anion is NO3; Cl stimulates the flux and, at constant Cl, NO3 inhibits it. Increase in the influx rate is rapid when shrunken ghosts are swollen or when NO3 is replaced by Cl. The volume-sensitive K influx requires intracellular MgATP at low concentrations, and ATP cannot be replaced by nonhydrolyzable ATP analogues. The volume-sensitive influx is inhibited by Mg2+ and by high concentrations of vanadate, but is stimulated by low concentrations of vanadate. It is not modified by cAMP, the removal of Ca2+ by EGTA, substances that activate protein kinase C, or by inhibition of phosphatidylinositol kinase. The influx is inhibited by neomycin and by trifluoperazine. |
format | Text |
id | pubmed-2228920 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1988 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-22289202008-04-23 Volume-sensitive K influx in human red cell ghosts J Gen Physiol Articles K influx into resealed human red cell ghosts increases when the ghosts are swollen. The influx demonstrates properties similar to volume- sensitive K fluxes present in other cells. The influx is, for the most part, insensitive to the nature of the major intracellular cation and therefore is not a K-K exchange. The influx is much greater when the major anion is Cl than when the major anion is NO3; Cl stimulates the flux and, at constant Cl, NO3 inhibits it. Increase in the influx rate is rapid when shrunken ghosts are swollen or when NO3 is replaced by Cl. The volume-sensitive K influx requires intracellular MgATP at low concentrations, and ATP cannot be replaced by nonhydrolyzable ATP analogues. The volume-sensitive influx is inhibited by Mg2+ and by high concentrations of vanadate, but is stimulated by low concentrations of vanadate. It is not modified by cAMP, the removal of Ca2+ by EGTA, substances that activate protein kinase C, or by inhibition of phosphatidylinositol kinase. The influx is inhibited by neomycin and by trifluoperazine. The Rockefeller University Press 1988-11-01 /pmc/articles/PMC2228920/ /pubmed/2853201 Text en This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Articles Volume-sensitive K influx in human red cell ghosts |
title | Volume-sensitive K influx in human red cell ghosts |
title_full | Volume-sensitive K influx in human red cell ghosts |
title_fullStr | Volume-sensitive K influx in human red cell ghosts |
title_full_unstemmed | Volume-sensitive K influx in human red cell ghosts |
title_short | Volume-sensitive K influx in human red cell ghosts |
title_sort | volume-sensitive k influx in human red cell ghosts |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2228920/ https://www.ncbi.nlm.nih.gov/pubmed/2853201 |