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Regulatory volume increase in rat pancreatic beta-cells
1Cell Physiology Group, School of Biological Sciences, Stopford Building, University of Manchester, Manchester M13 9PT, UK.
Pflugers Archiv : European Journal of Physiology
|February 7, 1998
Summary
Regulatory volume increase (RVI) in pancreatic beta-cells involves multiple transporters. Na+-2Cl--K+ cotransporters are key, but Na+-H+ and Cl--HCO3- exchangers also contribute to RVI in these cells.
Area of Science:
- Physiology
- Cell Biology
- Endocrinology
Background:
- Pancreatic beta-cells regulate cell volume, crucial for function.
- Regulatory Volume Increase (RVI) is a key volume regulatory mechanism.
- Understanding RVI in beta-cells is vital for insights into pancreatic function and disease.
Purpose of the Study:
- To investigate the transporters involved in regulatory volume increase (RVI) in rat pancreatic beta-cells.
- To differentiate the roles of various ion transport systems in beta-cell volume regulation.
Main Methods:
- Isolated rat pancreatic beta-cells were used.
- Cell volume changes were measured using a video-imaging method.
- Hypertonic solutions (100 mM mannitol) induced cell shrinkage, followed by RVI assessment.
Main Results:
- In HEPES-buffered solutions, RVI was largely abolished by bumetanide, indicating a major role for Na+-2Cl--K+ cotransporters.
- In HCO3--buffered solutions, a bumetanide-insensitive RVI component was observed.
- This component was inhibited by amiloride and DIDS, suggesting contributions from Na+-H+ and Cl--HCO3- exchangers.
Conclusions:
- Na+-2Cl--K+ cotransporters significantly contribute to RVI in pancreatic beta-cells.
- Functionally coupled Na+-H+ exchangers and Cl--HCO3- exchangers also play a role in beta-cell RVI, particularly in HCO3--buffered environments.