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This Article Full Text Full Text (PDF) All Versions of this Article: 586/21/5047    most recent jphysiol.2008.160440v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Berridge, M. J. PubMed PubMed Citation Articles by Berridge, M. J. Related Collections Review articles Cellular

¹ The Babraham Institute, Babraham, Cambridge CB22 4AT, UK

Smooth muscle cell (SMC) contraction is controlled by the Ca²⁺ and Rho kinase signalling pathways. While the SMC Rho kinase system seems to be reasonably constant, there is enormous variation with regard to the mechanisms responsible for generating Ca²⁺ signals. One way of dealing with this diversity is to consider how this system has been adapted to control different SMC functions. Phasic SMCs (vas deferens, uterus and bladder) rely on membrane depolarization to drive Ca²⁺ influx across the plasma membrane. This depolarization can be induced by neurotransmitters or through the operation of a membrane oscillator. Many tonic SMCs (vascular, airway and corpus cavernosum) are driven by a cytosolic Ca²⁺ oscillator that generates periodic pulses of Ca²⁺. A similar oscillator is present in pacemaker cells such as the interstitial cells of Cajal (ICCs) and atypical SMCs that control other tonic SMCs (gastrointestinal, urethra, ureter). The changes in membrane potential induced by these cytosolic oscillators does not drive contraction directly but it functions to couple together individual oscillators to provide the synchronization that is a characteristic feature of many tonic SMCs.

(Received 24 July 2008; accepted after revision 9 September 2008; first published online 11 September 2008)
Corresponding author M. J. Berridge: The Babraham Institute, Babraham, Cambridge CB22 4AT, UK. Email: michael.berridge{at}bbsrc.ac.uk