Ca2＋ plays a pivotal role in nitric oxide （NO）-promoted stomatal closure. However, the function of Ca2＋ in NO inhibition of blue light （BL）-induced stomatal opening remains largely unknown. Here, we analyzed the role of Ca2＋ in the crosstalk between BL and NO signaling in Vicia faba L. guard cells. Extracellular Ca2＋ modulated the BL-induced stomatal opening in a dose-dependent manner, and an application of 5 μM Ca2＋ in the pipette solution significantly inhibited BL-activated K＋ influx. Sodium nitroprusside （SNP）, a NO donor, showed little effect on BL-induced K＋ influx and stomatal opening response in the absence of extracellular Ca2＋ , but K＋ influx and stomatal opening were inhibited by SNP when Ca2＋ was added to the bath solution. Interestingly, although both SNP and BL could activate the plasma membrane Ca2＋ channels and induce the rise of cytosolic Ca2＋ , the change in levels of Ca2＋ channel activity and cytosolic Ca2＋ concentration were different between SNP and BL treatments. SNP at 100 μM obviously activated the plasma membrane Ca2＋ channels and induced cytosolic Ca2＋ rise by 102.4%. In contrast, a BL pulse （100 μmol/m 2 per s for 30 s） slightly activated the Ca2＋ channels and resulted in a Ca2＋ rise of only 20.8%. Consistently, cytosolic Ca2＋ promoted K＋ influx at 0.5 μM or below, and significantly inhibited K＋ influx at 5 μM or above. Taken together, our findings indicate that Ca2＋ plays dual and distinctive roles in the crosstalk between BL and NO signaling in guard cells, mediating both the BL-induced K＋ influx as an activator at a lower concentration and the NO-blocked K＋ influx as an inhibitor at a higher concentration.
