Calcium sparks in smooth muscle

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Abstract
Local intracellular Ca2+transients, termed Ca2+ sparks, are caused by the coordinated opening of a cluster of ryanodine-sensitive Ca2+ release channels in the sarcoplasmic reticulum of smooth muscle cells. Ca2+ sparks are activated by Ca2+ entry through dihydropyridine-sensitive voltage-dependent Ca2+ channels, although the precise mechanisms of communication of Ca2+ entry to Ca2+ spark activation are not clear in smooth muscle. Ca2+ sparks act as a positive-feedback element to increase smooth muscle contractility, directly by contributing to the global cytoplasmic Ca2+ concentration ([Ca2+]) and indirectly by increasing Ca2+ entry through membrane potential depolarization, caused by activation of Ca2+ spark-activated Cl− channels. Ca2+ sparks also have a profound negative-feedback effect on contractility by decreasing Ca2+ entry through membrane potential hyperpolarization, caused by activation of large-conductance, Ca2+-sensitive K+ channels. In this review, the roles of Ca2+sparks in positive- and negative-feedback regulation of smooth muscle function are explored. We also propose that frequency and amplitude modulation of Ca2+ sparks by contractile and relaxant agents is an important mechanism to regulate smooth muscle function.