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.
Wong
A Y
AY
Department of Physiology and Biophysics, Dalhousie University, Halifax, Canada.
Klassen
G A
GA
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