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In the smooth muscle, Ca2+-dependent ion channels are one of the effector molecules involved in physiologically important regulatory processes emploing Ca2+as a second messenger. These channels couple changes of [Ca2+]i in the vicinity of the cell plasma membrane to changes in membrane potential thus affecting voltage-gated ion channels and as a result the excitability of the cell. In this study, by combining fluorescence confocal imagine of [Ca2+]i with simultaneous recording of whole-cell current in voltage-clamped vascular myocytes we demonstrate that depending on the membrane voltage calcium sparks may evoke a burst of synchronous opening of either Ca2+ activated Cl- channels or Ca2+ -activated K+channels thus leading to the discharge of spontaneuos transient inward currents (STICs) or spontaneous transient outward current (STOCs), respectively. We show that comparative analysis of the amplitudes of calcium sparks and corresponding STOCs may be provide information about colocalisation between Ca2+-release channels (ryanodine receptors, RyRs) and clusters of Ca2+ -activated K+ channels. Propagating waves of elevated [Ca2+]i observed during membrane depolarization seem to arise from spatio-temporal recruitment of local Ca2+-release events. Similar to visceral myocytes, in vascular myocytes the spatial nonuniformity of sarcoplasmic reticulum and RyRs distribution within the cell may account for the existence of `frequent discharge sites` and the wide variation in the Ca2+ wave propagation velocities observed.