Human sperm are endowed with putative voltage dependent calcium channels (VDCC) that produce measurable increases in intracellular calcium ([Ca²⁺]_i) in response to membrane depolarization with potassium. These channels are blocked by nickel, inactivate in 1-2 minutes in calcium-deprived medium and are remarkably stimulated by NH₄Cl, suggesting a role for pHi. In a previous work, we have shown that the calcium permeability through these channels increases ~ 1-fold during in vitro "capacitation", a calcium - dependent process that sperm require to fertilize eggs. In this work, we have determined the pH_i- dependence of sperm VDCC. Simultaneous depolarization and pH_i alkalization with NH₄Cl induced an [Ca²⁺]_i increase that depended on the amount of NH₄Cl added. The VDCC stimulation as a function of pH_i showed a sigmoid curve in the 6.6-7.2 pHi range, with a half-maximum stimulation at pH ~ 7.00. At more alkaline pHi (= 7.3), a further stimulation occurred. Calcium release from internal stores did not contribute to the stimulating effect of pHi since the [Ca²⁺]_i increase induced by progesterone, that opens a calcium permeability pathway that does not involve gating of VDCC, was unaffected by ammonium. The ratio pHi-stimulated/non-stimulated calcium influx was nearly constant at different test depolarization values. Likewise, the depolarization-induced calcium influx in both pHi-stimulated and non-stimulated cells were equally blocked by nickel. In our capacitating conditions the pHi increased 0.11 pHi units suggesting that the calcium influx stimulation observed during sperm capacitation might be partially caused by pHi alkalization. Additionally, a calcium permeability pathway triggered exclusively by pHi alkalization was detected.