Three genes encoding T-type Ca²⁺ channels have been described but their correspondence to the various native T-type Ca²⁺ currents remains uncertain. In particular, Ca_v3.2 (or α_1H) was cloned from a human heart library, its message was found abundantly in cardiac tissue, and expressed Ca_v3.2 was shown to conduct low voltage-activated currents, which inactivate rapidly and are sensitive to Ni²⁺ and mibefradil. These observations suggested that Ca_v3.2 might encode native cardiac T-type Ca²⁺ channels but more information on the pharmacology of Ca_v3.2 was needed to confirm this hypothesis. In the present study, we compare the pharmacology of Ca_v3.2 expressed in HEK293 cells and of native T-type Ca²⁺ channels in guinea pig atrial myocytes ("native-T"). (1) Ca_v3.2 and native-T are insensitive to TTX and to toxins selective for N-, P-, or Q-type Ca²⁺ channels (ω-CTx-GVIA, ω-Aga-IVA, ω-CTx-MVIIC). (2) The half-maximal blocking concentration (IC₅₀) of mibefradil on Ca_v3.2 is near that on native-T and the block is similarly voltage-dependent. (3) Ca_v3.2 is five- to sixfold less sensitive than native-T to the 1,4-dihydropyridine (DHP) amlodipine, suggesting a difference in the DHP binding site. (4) Both channels display similar (but not identical) sensitivities to the inorganic blockers Ni²⁺ and Cd²⁺ and the IC₅₀s are in the range of values found for T-type Ca²⁺ currents in other cell types. (5) Ni²⁺ shifts the voltage dependence of Ca_v3.2 activation but not that of native-T. The many similarities between the two channels support the contention that Ca_v3.2 encodes cardiac T-type Ca²⁺ channels. The slight differences may be due to species variations and/or to the choice of splice variant.