Calcium events in smooth muscles and their interstitial cells; physiological roles of sparks

Authors


  • This report was presented at The Physiological Society Focused Meeting on Ion channels, genes and regulation in smooth muscle, at the University of Oxford, UK, 5–7 September 2005.

Corresponding author T. B. Bolton: Centre for Ion Channels and Cell Signalling, Basic Medical Sciences, St George's, University of London, London SW17 0RE, UK. Email: t.bolton@sghms.ac.uk

Abstract

The observation of spontaneous sporadic releases of packets of stored calcium made 20 years ago has opened up a number of new concepts in smooth muscle physiology: (1) the calcium release sites are ryanodine and inositol 1,4,5-trisphosphate (IP3) receptor channels which contribute to cell-wide increases in [Ca2+]i in response to cell depolarization, activation of IP3-generating receptors, or other stimuli; (2) changes in [Ca2+]i act back on the cell membrane to activate or modulate K+, Cl and cation channel activity so affecting contraction, in arterial smooth muscle for example affecting blood pressure; (3) IP3 production is voltage dependent and is believed to contribute to pacemaker potentials and to refractory periods which control the rhythmical motility of many hollow organs. Most smooth muscle tissues contain interstitial cells (ICs) in addition to contractile smooth muscle cells (SMCs). The interactions of these internal mechanisms, and in turn the interactions of SMCs and ICs in various smooth muscle tissues, are major factors in determining the unique physiological profiles of individual smooth muscles.

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