Orai1, STIM1, and iPLA2β Determine Arterial Vasoconstriction
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There is no need to emphasize the role of Ca2+ entry as one of the major factors that determine constriction of arterial smooth muscle cells (SMC).1 For many years voltage-gated Ca2+ channels were thought to be a main path for Ca2+ entry, but recently it became clear that a variety of other Ca2+-conducting channels exist in vascular SMC, can respond to contractile agonists, and may play important roles in cardiovascular function.2–4 One of them is a store-operated channel (SOC) that many thought to be critically important only for store-operated Ca2+ entry (SOCE) in nonexcitable cells (that lack voltage-gated Ca2+ channels) but recently made its triumphant breakthrough into the reality of the excitable cells. Presently there is no doubt that SOCE is involved in SMC function,5,6 but debate continues on whether molecular determinants and mechanism of SOCE found in nonexcitable cells and heterologous systems may be directly applied to vascular SMC. It also remains unclear how important SOCE mechanism is for responses of small pressurized vessels to physiologically relevant vasoconstrictors and how it relates to voltage-gated Ca2+ channels.
See accompanying article on page 1325
In nonexcitable cells SOCE is mediated by Ca2+ …