ABSTRACT _1H T-type channels recruited by 1-adrenergic stimulation in rat chromaffin cells (RCCs) are coupled to fast exocytosis with the same Ca²⁺-dependence of high-threshold Ca²⁺ channels. Here we show that RCCs exposed to chronic hypoxia (12-18 h, 3% O2) express comparable densities of functional T-type channels that depolarize the resting cells and contribute to low-voltage exocytosis. Following chronic hypoxia, most RCCs exhibited Ca²⁺ channels already available at –50 mV with the same gating, pharmacological and molecular features of _1H isoform. Availability of T-type channels in hypoxic RCCs was revealed by lower resting potentials with respect to controls (–59 vs –66 mV in 4 mM KCl) and by small hyperpolarizations (5-8 mV) that accompanied the block of a T-type "window-current" with 50 µM Ni²⁺. Chronic hypoxia had no effects on cell size and high-threshold Ca²⁺ current density and was mimicked by overnight incubation with the iron-chelating agent desferrioxamine (DFX), suggesting the involvement of hypoxia-inducible factors (HIFs). T-type channel recruitment occurred independently of PKA-activation and extracellular Ca²⁺. The secretory response associated with Ca²⁺-influx through T-type channels could be detected following mild stimulations, either by depolarization-evoked capacitance increases or by amperometric current spikes induced by KCl-solutions. In the latter case, exocytotic bursts could be evoked right from low-KCl concentrations (2-4 mM) and spikes frequency was drastically reduced by 50 µM Ni²⁺. Chronic hypoxia did not alter the kinetics of spikes, suggesting that hypoxia-recruited T-type channels increase the number of secreted vesicles at low-voltages, without altering the mechanism of catecholamine release and the quantal content of released molecules. _1H T-type channels recruited by 1-adrenergic stimulation in rat chromaffin cells (RCCs) are coupled to fast exocytosis with the same Ca²⁺-dependence of high-threshold Ca²⁺ channels. Here we show that RCCs exposed to chronic hypoxia (12-18 h, 3% O2) express comparable densities of functional T-type channels that depolarize the resting cells and contribute to low-voltage exocytosis. Following chronic hypoxia, most RCCs exhibited Ca²⁺ channels already available at –50 mV with the same gating, pharmacological and molecular features of _1H isoform. Availability of T-type channels in hypoxic RCCs was revealed by lower resting potentials with respect to controls (–59 vs –66 mV in 4 mM KCl) and by small hyperpolarizations (5-8 mV) that accompanied the block of a T-type "window-current" with 50 µM Ni²⁺. Chronic hypoxia had no effects on cell size and high-threshold Ca²⁺ current density and was mimicked by overnight incubation with the iron-chelating agent desferrioxamine (DFX), suggesting the involvement of hypoxia-inducible factors (HIFs). T-type channel recruitment occurred independently of PKA-activation and extracellular Ca²⁺. The secretory response associated with Ca²⁺-influx through T-type channels could be detected following mild stimulations, either by depolarization-evoked capacitance increases or by amperometric current spikes induced by KCl-solutions. In the latter case, exocytotic bursts could be evoked right from low-KCl concentrations (2-4 mM) and spikes frequency was drastically reduced by 50 µM Ni²⁺. Chronic hypoxia did not alter the kinetics of spikes, suggesting that hypoxia-recruited T-type channels increase the number of secreted vesicles at low-voltages, without altering the mechanism of catecholamine release and the quantal content of released molecules