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HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas

Ion transport activity in pancreatic α-cells was assessed by studying cell volume regulation in response to anisotonic solutions. Cell volume was measured by a video imaging method, and cells were superfused with either 4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid-buffered or HCO(3)(−)-buffere...

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Detalles Bibliográficos
Autores principales: Davies, Sarah L., Best, Len, Brown, Peter D.
Formato: Texto
Lenguaje:English
Publicado: Springer-Verlag 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2691524/
https://www.ncbi.nlm.nih.gov/pubmed/19214560
http://dx.doi.org/10.1007/s00424-009-0644-4
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author Davies, Sarah L.
Best, Len
Brown, Peter D.
author_facet Davies, Sarah L.
Best, Len
Brown, Peter D.
author_sort Davies, Sarah L.
collection PubMed
description Ion transport activity in pancreatic α-cells was assessed by studying cell volume regulation in response to anisotonic solutions. Cell volume was measured by a video imaging method, and cells were superfused with either 4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid-buffered or HCO(3)(−)-buffered solutions. α-Cells did not exhibit a regulatory volume increase (RVI) in response to cell shrinkage caused by hypertonic solutions. A RVI was observed, however, in cells that had first undergone a regulatory volume decrease (RVD), but only in HCO(3)(−)-buffered solutions. RVI was also observed in response to a HCO(3)(−)-buffered hypertonic solution in which the glucose concentration was increased from 4 to 20 mM. The post-RVD RVI and the glucose-induced RVI were both inhibited by 10 μM 5-(N-methyl-N-isobutyl) amiloride or 100 μM 2,2′-(1,2-ethenediyl) bis (5-isothio-cyanatobenzenesulfonic acid), but not by 10 μM benzamil nor 10 μM bumetanide. These data suggest that Na(+)–H(+) exchangers and Cl(−)–HCO(3)(−) exchangers contribute to volume regulation in α-cells.
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spelling pubmed-26915242009-06-05 HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas Davies, Sarah L. Best, Len Brown, Peter D. Pflugers Arch Transport Physiology Ion transport activity in pancreatic α-cells was assessed by studying cell volume regulation in response to anisotonic solutions. Cell volume was measured by a video imaging method, and cells were superfused with either 4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid-buffered or HCO(3)(−)-buffered solutions. α-Cells did not exhibit a regulatory volume increase (RVI) in response to cell shrinkage caused by hypertonic solutions. A RVI was observed, however, in cells that had first undergone a regulatory volume decrease (RVD), but only in HCO(3)(−)-buffered solutions. RVI was also observed in response to a HCO(3)(−)-buffered hypertonic solution in which the glucose concentration was increased from 4 to 20 mM. The post-RVD RVI and the glucose-induced RVI were both inhibited by 10 μM 5-(N-methyl-N-isobutyl) amiloride or 100 μM 2,2′-(1,2-ethenediyl) bis (5-isothio-cyanatobenzenesulfonic acid), but not by 10 μM benzamil nor 10 μM bumetanide. These data suggest that Na(+)–H(+) exchangers and Cl(−)–HCO(3)(−) exchangers contribute to volume regulation in α-cells. Springer-Verlag 2009-02-13 2009-07 /pmc/articles/PMC2691524/ /pubmed/19214560 http://dx.doi.org/10.1007/s00424-009-0644-4 Text en © The Author(s) 2009
spellingShingle Transport Physiology
Davies, Sarah L.
Best, Len
Brown, Peter D.
HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
title HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
title_full HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
title_fullStr HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
title_full_unstemmed HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
title_short HCO(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
title_sort hco(3)(−)-dependent volume regulation in α-cells of the rat endocrine pancreas
topic Transport Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2691524/
https://www.ncbi.nlm.nih.gov/pubmed/19214560
http://dx.doi.org/10.1007/s00424-009-0644-4
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