The receptor mechanism of testosterone‐induced nongenomic Ca²⁺ signaling in prostate cancer cells is poorly understood. In this study we investigated androgen‐induced intracellular Ca²⁺ increases in LNCaP human prostate cancer cells with Fura‐2 as a Ca²⁺ probe. 5α‐dihydrotestosterone (DHT) produced fast and transient increases in intracellular Ca²⁺ in LNCaP cells in a concentration‐dependent manner. These effects were abolished by extracellular Ca²⁺ removal or pretreatment with L‐type Ca²⁺ channel inhibitors (nifedipine, verapamil, and diltiazem). Pretreatment with endoplasmic reticulum ryanodine receptor blocker (procaine) or phospholipase C inhibitor (neomycin sulfate) did not alter DHT‐induced Ca²⁺ influx. The concentration of Ca²⁺ was also increased by impermeable testosterone conjugated to bovine serum albumin. Neither an antagonist of intracellular androgen receptors (cyproterone acetate) nor a protein synthesis inhibitor (cycloheximide) affected this fast Ca²⁺ influx. Furthermore, the effect of DHT was abolished in cells incubated with a G protein inhibitor (pertussis toxin) and a nonhydrolyzable analog of guanosine triphosphate (guanosine 5‐[b‐thio]disphosphate) but not in cells incubated with the tyrosine kinase inhibitor genistein. These results indicate that androgens induced an L‐type calcium channel—dependent intracellular Ca²⁺ increase in LNCaP prostate cancer cells. The rapid responses triggered by DHT did not appear to be mediated through classic intracellular androgen receptors, c‐Src kinase‐androgen receptor complex, or sex hormone—binding globulin but through a G protein—coupled receptor in LNCaP prostate cancer cells. These results may provide a new explanation for progression of prostate cancer.