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Furosemide stimulates K transport in HCD57 erythroid cells
H D Kim1, J T Turner, J E Burnett
1Department of Pharmacology, University of Missouri, M517B Medical Sciences Building, One Hospital Center Dr., Columbia, MO 65212, USA.
The Journal of Membrane Biology
|June 2, 2000
Summary
Serum concentration critically affects cell volume in HCD57 cells, influencing potassium (K) movement. Furosemide
Area of Science:
- Cell Biology
- Physiology
- Biochemistry
Background:
- HCD57 cells, a murine erythroleukemia line, require erythropoietin (EPO) for survival.
- Cell volume regulation is crucial for cellular function and survival.
- Serum concentration is known to influence cellular processes.
Purpose of the Study:
- To investigate the effects of serum and furosemide on potassium (K) movement and cell volume in HCD57 cells.
- To elucidate the role of K permeability in cell volume regulation.
- To understand the dual action of furosemide on K uptake.
Main Methods:
- Culturing HCD57 cells in media with varying serum concentrations.
- Manipulating external potassium (K) concentrations.
- Assessing cell volume changes and K uptake in the presence and absence of furosemide.
Main Results:
- Cell volume maintenance is dependent on serum concentration; reduced serum leads to cell shrinkage.
- In serum-free conditions, elevated external K prevents shrinkage and high K induces swelling, indicating K permeability's role.
- Furosemide inhibits K uptake at low external K (2% serum) but stimulates it dose-dependently at higher concentrations.
- Furosemide potentiates serum withdrawal-induced cell shrinkage.
Conclusions:
- Serum concentration is a key regulator of HCD57 cell volume.
- Potassium (K) transport is integral to cell volume homeostasis.
- Furosemide exhibits a concentration-dependent biphasic effect on K uptake, influencing cell volume regulation.
- Cellular shrinkage mechanisms can be modulated by external stimuli like furosemide after initial priming by serum depletion.