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.