Local increases in intracellular calcium ion concentration ([Ca²⁺]_i) resulting from activation of the ryanodine-sensitive calcium-release channel in the sarcoplasmic reticulum (SR) of smooth muscle cause arterial dilation. Ryanodine-sensitive, spontaneous local increases in [Ca²⁺]_i (Ca²⁺ sparks) from the SR were observed just under the surface membrane of single smooth muscle cells from myogenic cerebral arteries. Ryanodine and thapsigargin inhibited Ca²⁺ sparks and Ca²⁺-dependent potassium (K_Ca) currents, suggesting that Ca²⁺ sparks activate K_Ca channels. Furthermore, K_Ca channels activated by Ca²⁺ sparks appeared to hyperpolarize and dilate pressurized myogenic arteries because ryanodine and thapsigargin depolarized and constricted these arteries to an extent similar to that produced by blockers of K_Ca channels. Ca²⁺ sparks indirectly cause vasodilation through activation of K_Ca channels, but have little direct effect on spatially averaged [Ca²⁺]_i, which regulates contraction.