A model of cytosolic calcium regulation and autacoids production in vascular endothelial cell.
A model of vascular endothelial cell is proposed to describe the mechanisms by which cytosolic calcium (Cai) is modulated and endothelium-derived relaxing factor (EDRF) and prostacyclin (PGI2) are released when the cell is stimulated by agonist. The intracellular Ca2+ store of the model cell is comprised of a superficial (sc) and a deep (dc) compartment. The dc Ca2+ content is refilled by the sc whose [Ca2+] is the same as extracellular Ca2+. Inositol (1,4,5)-trisphosphate (IP3) produced by agonist modifies the dc permeability which discharges its Ca2+ to the cytosol. The increase of Cai induces Ca2+ released from the sc. Ca(2+)-activated K+ current hyperpolarises the cell. The raised Cai releases PGI2 in the presence of IP3 while EDRF is released by Cai. The model explains satisfactorily the Ca2+ transient and autacoids production of the aortic endothelial cell without the need of calcium influx from extracellular space. The cytoplasmic Ca2+ oscillations observed in human endothelial cell from umbilical veins were reproduced by the model. Production of EDRF by the artery due to increase in pressure was also simulated.
Department of Physiology and Biophysics, Dalhousie University, Halifax, Canada.
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Wong
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D012898:Autacoids / Q000096:biosynthesis*; D002118:Calcium / Q000378:metabolism*; D002451:Cell Compartmentation; D003600:Cytosol / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D011464:Epoprostenol / Q000378:metabolism; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D008433:Mathematics; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism
D012898:Autacoids; D009569:Nitric Oxide; D015544:Inositol 1,4,5-Trisphosphate; D011464:Epoprostenol; D002118:Calcium