This Article Full Text Full Text (PDF) All Versions of this Article: biophysj.104.054965v1 88/6/3845    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Koenigsberger, M. Articles by Meister, J.-J. Search for Related Content PubMed PubMed Citation Articles by Koenigsberger, M. Articles by Meister, J.-J.

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.

This article has been cited by other articles:

				M. Koenigsberger, R. Sauser, D. Seppey, J.-L. Beny, and J.-J. Meister Calcium Dynamics and Vasomotion in Arteries Subject to Isometric, Isobaric, and Isotonic Conditions Biophys. J., September 15, 2008; 95(6): 2728 - 2738. [Abstract] [Full Text] [PDF]

				J.-L. Beny, M. Koenigsberger, and R. Sauser Role of myoendothelial communication on arterial vasomotion Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2036 - H2038. [Full Text] [PDF]

				M. Koenigsberger, R. Sauser, J.-L. Beny, and J.-J. Meister Effects of Arterial Wall Stress on Vasomotion Biophys. J., September 1, 2006; 91(5): 1663 - 1674. [Abstract] [Full Text] [PDF]

				R. E Haddock and C. E Hill Rhythmicity in arterial smooth muscle J. Physiol., August 1, 2005; 566(3): 645 - 656. [Abstract] [Full Text] [PDF]