Modelling the electrophysiological endothelial cell response to bradykinin.

Schuster A; Bény JL; Meister JJ

doi:10.1007/s00249-003-0279-x

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Journal article

Modelling the electrophysiological endothelial cell response to bradykinin.

Schuster A Cellular Biophysics and Biomechanics Laboratory, Swiss Federal Institute of Technology, 1015, Lausanne, Switzerland. schuster@bioeng.ucsd.edu
Bény JL
Meister JJ

2003-07-10

Published in:

European biophysics journal : EBJ. - 2003

English 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.

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