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lüll Store-operated calcium entry in vascular smooth muscle Leung FP; Yung LM; Yao X; Laher I; Huang YBr J Pharmacol 2008[Mar]; 153 (5): 846-57In non-excitable cells, activation of G-protein-coupled phospholipase C (PLC)-linked receptors causes the release of Ca(2+) from intracellular stores, which is followed by transmembrane Ca(2+) entry. This Ca(2+) entry underlies a small and sustained phase of the cellular [Ca(2+)](i) increases and is important for several cellular functions including gene expression, secretion and cell proliferation. This form of transmembrane Ca(2+) entry is supported by agonist-activated Ca(2+)-permeable ion channels that are activated by store depletion and is referred to as store-operated Ca(2+) entry (SOCE) and represents a major pathway for agonist-induced Ca(2+) entry. In excitable cells such as smooth muscle cells, Ca(2+) entry mechanisms responsible for sustained cellular activation are normally considered to be mediated via either voltage-operated or receptor-operated Ca(2+) channels. Although SOCE occurs following agonist activation of smooth muscle, this was thought to be more important in replenishing Ca(2+) stores rather than acting as a source of activator Ca(2+) 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.|Animals[MESH]|Calcium Channels/*metabolism[MESH]|Calcium-Transporting ATPases/antagonists & inhibitors[MESH]|Calcium/*metabolism[MESH]|Cardiovascular Diseases/physiopathology[MESH]|Cardiovascular Physiological Phenomena[MESH]|Cell Membrane[MESH]|Drug Delivery Systems[MESH]|Humans[MESH]|Muscle, Smooth, Vascular/*metabolism[MESH] |