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 (Ca(i)) 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 Ca(i) induces Ca2+ released from the sc. Ca2+-activated K+ current hyperpolarises the cell. The raised Ca(i) releases PGI2 in the presence of IP3 while EDRF is released by Ca(i). 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.