Smooth muscle cell calcium activation mechanisms

• Published in: The Journal of physiology 2008-11, Vol.586 (21), p.5047-5061
• Main Author: Berridge, Michael J.
• Format: Article
• Language: English
• Subjects: Animals; Calcium Signaling - physiology; Humans; Membrane Potentials; Mice; Myocytes, Smooth Muscle - metabolism; Topical Review
• ISSN: 0022-3751; 1469-7793
• DOI: 10.1113/jphysiol.2008.160440

Smooth muscle cell (SMC) contraction is controlled by the Ca 2+ 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 Ca 2+ 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 Ca 2+ 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 Ca 2+ oscillator that generates periodic pulses of Ca 2+ . 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.