Contraction of vascular smooth muscle cells (VSMCs) depends on the rise of cytosolic [Ca²⁺] owing to either Ca²⁺ influx or release from the sarcoplasmic reticulum (SR). We have shown that, in the absence of transmembrane Ca²⁺ influx, activation of L-type Ca²⁺ channels regulates Ca²⁺ release from the SR. We denoted Ca²⁺ channel-SR coupling as Ca²⁺ channel induced calcium release (CCICR). In current clamped, dispersed rat basilar myocytes (bathed in O Ca²⁺ solution) depolarization by high extracellular K⁺ evoked a fast Ca²⁺ release signal. A similar response was elicited in voltage-clamped cells by depolarizing pulses. These results suggested that membrane depolarization was sensed by Ca²⁺ channels, which in turn induced Ca²⁺ release from SR. Consistent with this proposal, organic Ca²⁺ channel agonists (Bay-K and FPL) induced CCICR, whereas Ca²⁺ channel antagonists (such as nifedipine, diltiazem or D600) blocked CCICR. CCICR was abolished upon pharmacological inhibition of phospholipase C, suppression of G-protein activation by intracellular GDP-bS, or inhibition of Ca²⁺ release channels. Several conditions, as for example elevation in extracellular ATP or hypoxia can modulate CCICR. These observations demonstrate a new mechanism of signaling SR Ca²⁺-release channels and reveal an unexpected metabotropic function of voltage-gated Ca²⁺ channels in arterial myocytes.