Store‐operated calcium entry in vascular smooth muscle

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Abstract
In non‐excitable cells, activation of G‐protein‐coupled phospholipase C (PLC)‐linked receptors causes the release of Ca2+from intracellular stores, which is followed by transmembrane Ca2+entry. This Ca2+entry underlies a small and sustained phase of the cellular [Ca2+]iincreases and is important for several cellular functions including gene expression, secretion and cell proliferation. This form of transmembrane Ca2+entry is supported by agonist‐activated Ca2+‐permeable ion channels that are activated by store depletion and is referred to as store‐operated Ca2+entry (SOCE) and represents a major pathway for agonist‐induced Ca2+entry. In excitable cells such as smooth muscle cells, Ca2+entry mechanisms responsible for sustained cellular activation are normally considered to be mediated via either voltage‐operated or receptor‐operated Ca2+channels. Although SOCE occurs following agonist activation of smooth muscle, this was thought to be more important in replenishing Ca2+stores rather than acting as a source of activator Ca2+for the contractile process. This review summarizes our current knowledge of SOCE as a regulator of vascular smooth muscle tone and discusses its possible role in the cardiovascular function and disease. We propose a possible hypothesis for its activation and suggest that SOCE may represent a novel target for pharmacological therapeutic intervention.British Journal of Pharmacology(2008)153, 846–857; doi:10.1038/sj.bjp.0707455; published online 17 September 2007