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Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells
Published on: July 16, 2013
Caffeine activates a mechanosensitive Ca(2+) channel in human red cells
1Laboratory of Membrane Physiology, Faculty of Sciences, Institute of Experimental Biology, Central University of Venezuela, Aptdo. 47114, Caracas 1041-A, Venezuela.
Cell Calcium
|July 6, 2002
Summary
Caffeine stimulates cation channels in human red blood cells, specifically activating calcium (Ca2+) influx. Aged cells show reduced susceptibility to these caffeine-induced channel blockers.
Area of Science:
- Cell Biology
- Biophysics
- Physiology
Background:
- Caffeine is known to activate cation influx in various cell types.
- This suggests caffeine may open non-selective cation channels in the plasma membrane.
Purpose of the Study:
- To investigate caffeine's action on cation movements (Ca2+, Na+, K+) in human erythrocytes.
- To determine if caffeine activates stretch-activated cation channels.
Main Methods:
- Studied net cation fluxes in ATP-depleted human erythrocytes (young and old).
- Tested caffeine's effects in the presence of mechanosensitive channel blockers (Gd3+, neomycin, amiloride) and ruthenium red.
- Compared caffeine-induced cation influx with hypotonicity-induced influx.
Main Results:
- Caffeine enhanced net cation fluxes in a concentration-dependent manner.
- Caffeine-stimulated Ca2+ entry was suppressed by Gd3+, amiloride, and ruthenium red, and partially by neomycin.
- Inhibitors blocked caffeine-dependent Na+ entry and showed antagonistic effects on K+ efflux.
- Inhibitors blocked hypotonicity-induced Ca2+ influx at similar concentrations.
- Young erythrocytes were more susceptible to inhibitors than old erythrocytes.
Conclusions:
- Caffeine stimulates a stretch-activated Ca2+ channel in human red blood cells.
- Aged erythrocytes are less susceptible to mechanosensitive channel blockers compared to young cells.
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