Ca²⁺ sparks have been previously described in isolated smooth muscle cells. Here we present the first measurements of local Ca²⁺ transients (“Ca²⁺ sparks”) in an intact smooth muscle preparation. Ca²⁺sparks appear to result from the opening of ryanodine-sensitive Ca²⁺ release (RyR) channels in the sarcoplasmic reticulum (SR). Intracellular Ca²⁺ concentration ([Ca²⁺]_i) was measured in intact cerebral arteries (40–150 μm in diameter) from rats, using the fluorescent Ca²⁺ indicator fluo 3 and a laser scanning confocal microscope. Membrane potential depolarization by elevation of external K⁺ from 6 to 30 mM increased Ca²⁺ spark frequency (4.3-fold) and amplitude (∼2-fold) as well as global arterial wall [Ca²⁺]_i(∼1.7-fold). The half time of decay (∼50 ms) was not affected by membrane potential depolarization. Ryanodine (10 μM), which inhibits RyR channels and Ca²⁺ sparks in isolated cells, and thapsigargin (100 nM), which indirectly inhibits RyR channels by blocking the SR Ca²⁺-ATPase, completely inhibited Ca²⁺ sparks in intact cerebral arteries. Diltiazem, an inhibitor of voltage-dependent Ca²⁺ channels, lowered global [Ca²⁺]_iand Ca²⁺ spark frequency and amplitude in intact cerebral arteries in a concentration-dependent manner. The frequency of Ca²⁺sparks (<1 s⁻¹ ⋅ cell⁻¹), even under conditions of steady depolarization, was too low to contribute significant amounts of Ca²⁺ to global Ca²⁺ in intact arteries. These results provide direct evidence that Ca²⁺ sparks exist in quiescent smooth muscle cells in intact arteries and that changes of membrane potential that would simulate physiological changes modulate both Ca²⁺ spark frequency and amplitude in arterial smooth muscle.