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 aortie 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 pressre also simulated.