Schuster A Bény JL Meister JJ 2003 The goal of the present study is to construct a biophysical model of the coronary artery endothelial cell response to bradykinin. This model takes into account intracellular Ca2+ dynamics, membrane potential, a non-selective cation channel, and two Ca(2+)-dependent K+ channels, as well as intra- and extracellular Ca2+ sources. The model reproduces the experimental data available, and predicts certain quantities which would be hard to obtain experimentally, like the individual K+ channel currents when the membrane potential is allowed to freely evolve, the implication of epoxyeicosatrienoic acids (EETs), and the total K+ released during stimulation. The main results are: (1) the large-conductance K+ channel participates only very little in the overall response; (2) EETs are required in order to explain the experimental current-potential relationships, but are not an essential component of the bradykinin response; and (3) the total K+ released during stimulation gives rise to a concentration in the intercellular space which is of millimolar order. This concentration change is compatible with the hypothesis that K+ contributes to the endothelium-derived hyperpolarizing factor phenomenon. application/pdf https://sonar.ch/global/documents/212409 eng info:eu-repo/semantics/altIdentifier/doi/10.1007/s00249-003-0279-x info:eu-repo/semantics/altIdentifier/pmid/12851795 info:eu-repo/semantics/openAccess European biophysics journal : EBJ. - 2003 Animals Arteries Bradykinin Calcium Calcium Signaling Coronary Vessels Electrophysiology Endothelium, Vascular Ion Channel Gating Membrane Potentials Models, Cardiovascular Potassium Channels Reproducibility of Results Sensitivity and Specificity Swine Modelling the electrophysiological endothelial cell response to bradykinin. http://purl.org/coar/resource_type/c_6501