To investigate the mechanism of extracellular Ca 2+ in alleviating salt stress, the effects of Ca 2+ on stomatal movement and K + channels in Vicia faba under 100 mmol L −1 NaCl stress were studied using electrophysiological and cytobiological techniques. Under NaCl stress, the stomata were induced to open. Extracellular Ca 2+ facilitated the phenomena at a concentration of 0.1 mmol L −1 and significantly inhibited it at a concentration of 10 mmol L −1. To gain further insights into Ca 2+ function in NaCl-regulated stomatal movement, V. faba guard cell protoplasts were patch-clamped in a whole-cell configuration. Ca 2+ significantly inhibited both inward and outward rectifying K + currents when CaCl 2 was added to the bath solution at concentration of 10 mmol L −1 under NaCl stress, which was alleviated by La 3+ (a inhibitor of plasma membrane Ca 2+ channel) at concentration of 1 mmol L −1. In contrast, 10 mmol L −1 CaCl 2 significantly inhibited inward rectifying K + currents and activated outward rectifying K + currents under natural conditions, which was not alleviated by La 3+. A single-cell analysis of cytosolic H 2O 2 using 2′,7′-dichlorofluorescin (H 2DCF-DA) revealed that extracellular Ca 2+ induced the generation of H 2O 2 in the guard cells with 10 mmol L −1 CaCl 2 under NaCl stress, but 10 mmol L −1 CaCl 2 or 100 mmol L −1 NaCl had few effects on the accumulation of H 2O 2 in the guard cells. These results suggest that extracellular Ca 2+ may alleviate the damage caused by NaCl stress through inducing the production of H 2O 2, accordingly, the H 2O 2-activated increase in cytosolic free Ca 2+ concentration ([Ca 2+] cyt) reduces Na + uptake through regulating plasma membrane K + channels in guard cells. These effects lead to stomatal closure and reduction of water loss.