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Biophys. J. BioFAST: First Published March 25, 2005. doi:10.1529/biophysj.104.054965
© 2005 by the Biophysical Society.

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BIOPHYSICAL THEORY AND MODELING

Role of the endothelium on arterial vasomotion

Michéle Koenigsberger 1*, Roger Sauser 1, Jean-Louis Beny 2 and Jean-Jacques Meister 1

1 Ecole polytechnique fédérale Lausanne (EPFL)
2 University of Geneva

* To whom correspondence should be addressed. E-mail: michele.koenigsberger{at}epfl.ch.

Submitted on October 22, 2004
Revised on December 23, 2004
Accepted on 22 March 2005


  Abstract
It is well-known that cyclic variations of the vascular diameter, a phenomenon called vasomotion, are induced by synchronous calcium oscillations of smooth muscle cells (SMCs). However, the role of the endothelium on vasomotion is unclear. Some experimental studies claim that the endothelium is necessary for synchronization and vasomotion, whereas others report rhythmic contractions in absence of an intact endothelium. Moreover, endothelium derived factors have been shown to abolish vasomotion by desynchronizing the calcium signals in SMCs. By modeling the calcium dynamics of a population of SMCs coupled to a population of endothelial cells, we analyze the effects of an SMC vasoconstrictor stimulation on endothelial cells and the feedback of endothelium derived factors. Our results show that the endothelium essentially decreases the SMCs calcium level and may move the SMCs from a steady state to an oscillatory domain, and vice versa. In the oscillatory domain, a population of coupled SMCs exhibits synchronous calcium oscillations. Outside the oscillatory domain, the coupled SMCs present only irregular calcium flashings arising from noise modeling stochastic opening of channels. Our findings provide explanations for the published contradictory experimental observations.

Key Words: artery, calcium oscillations, cellular communication, model, smooth muscle cells, synchronization




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Copyright © 2005 by the Biophysical Society.