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.