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Role of the Endothelium on Arterial Vasomotion

Michèle Koenigsberger ^*, Roger Sauser ^*, Jean-Louis Bény  and Jean-Jacques Meister ^*

^* Ecole Polytechnique Fédérale de Lausanne, Laboratory of Cell Biophysics, Lausanne, Switzerland; and Department of Zoology and Animal Biology, University of Geneva, Geneva, Switzerland

Correspondence: Address reprint requests to Michèle Koenigsberger, Ecole Polytechnique Fédérale de Lausanne (EPFL), Laboratory of Cell Biophysics, CH-1015 Lausanne, Switzerland. Tel.: 41-21-693-8347; Fax: 41-21-693-8305; E-mail: michele.koenigsberger{at}epfl.ch.

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 the 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.

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