We have defined Ca²⁺ channel subtypes expressed in rabbit carotid body (CB) chemoreceptor cells and their participation in the stimulus‐evoked catecholamine (CA) release. Ca²⁺ currents (I_Ca) activated at –30 mV, peaked at +10 mV and were fully blocked by 200 μm Cd²⁺. L‐type channels (sensitive to 2 μm nisoldipine) activated at –30 mV and carried 21 ± 2% of total I_Ca. Non‐L‐type channels activated at potentials positive to –10 mV and carried: N channels (sensitive to 1 μmω‐conotoxin‐GVIA) 16 ± 1% of total I_Ca, P/Q channels (sensitive to 3 μmω‐conotoxin‐MVIIC after nisoldipine plus GVIA) 23 ± 3% of total I_Ca and R channels (resistant to all blockers combined) 40 ± 3% of total I_Ca. CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high K⁺_o in the intact CB was inhibited by 79–98% by 200 μm Cd²⁺. Hypoxia, hypercapnic acidosis and DNP, depolarized chemoreceptor cells and eventually generated repetitive action potential discharge. Nisoldipine plus MVIIC nearly abolished the release of CAs induced by hypoxia and hypercapnic acidosis and reduced by 74% that induced by DNP. All these secretory responses were insensitive to GVIA. 30 and 100 mm K⁺_o brought resting membrane potential (E_m) of chemoreceptor cells (–48.1 ± 1.2 mV) to –22.5 and +7.2 mV, respectively. Thirty millimolar K⁺_o‐evoked release was abolished by nisoldipine but that induced by 100 mm K⁺_o was mediated by activation of L, N, and P/Q channels. Data show that tested stimuli depolarize rabbit CB chemoreceptor cells and elicit CA release through Ca²⁺ entry via voltage‐activated channels. Only L and P/Q channels are tightly coupled to the secretion of CA.