| Reference : Cholesterol and its oxidized derivatives modulate the calcium channel in human red bl... |
| Scientific journals : Article | |||
| Human health sciences : Cardiovascular & respiratory systems | |||
| http://hdl.handle.net/10993/27471 | |||
| Cholesterol and its oxidized derivatives modulate the calcium channel in human red blood cells. | |
| English | |
Neyses, Ludwig  [University of Luxembourg > Research Office] | |
| Stimpel, M. [> >] | |
| Locher, R. [> >] | |
| Streuli, R. [> >] | |
| Kuffer, B. [> >] | |
| Vetter, W. [> >] | |
| 1984 | |
| Journal of Hypertension. Supplement) | |
| 2 | |
| 3 | |
| S489-92 | |
| Yes (verified by ORBilu) | |
| International | |
| 0952-1178 | |
| ENGLAND | |
| [en] Calcium/blood ; Cholesterol/analogs & derivatives/blood/pharmacology ; Dose-Response Relationship, Drug ; Erythrocytes/drug effects/metabolism ; Humans ; Ion Channels/drug effects/metabolism ; Oxidation-Reduction | |
| [en] The human red blood cell was used as a model system in order to study the effect of cholesterol and its medically important oxidized derivatives (OSC = oxidized sterol compounds) on the calcium entry channel. The calcium-ejecting adenosine triphosphatase (ATPase) was inhibited by vanadate and the influx of 45Ca2-into the cells measured. The cells were loaded with OSC at concentrations between 0.075 and 1.5 micrograms OSC/10(7) cells. Two classes of OSC could be distinguished: one stimulating Ca2+ influx dose-dependently by almost 100% at maximum concentrations, the other inhibiting it dose-dependently by up to 80%. The calcium channel blocker nitrendipine inhibited influx by 70% at 15 microM. More than 90% of the total stimulation or inhibition was accounted for by an influence on the nitrendipine-inhibitable part of influx, i.e. the calcium channel. Cholesterol (incorporated using liposomes) had a stimulatory (+288%), cholesterol depletion an inhibitory effect on calcium influx (-18%). These results demonstrate that cholesterol and its oxidized derivatives modulate the calcium channel in a highly stereospecific manner and provide new insights into the mechanism of action and the atherogenic effect of these compounds. | |
| http://hdl.handle.net/10993/27471 |
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