Nitric Oxide Blocks Blue Light‐Induced K + Influx by Elevating the Cytosolic Ca 2+ Concentration in Vicia faba L. Guard Cells

Ca 2+ plays a pivotal role in nitric oxide (NO)‐promoted stomatal closure. However, the function of Ca 2+ in NO inhibition of blue light (BL)‐induced stomatal opening remains largely unknown. Here, we analyzed the role of Ca 2+ in the crosstalk between BL and NO signaling in Vicia faba L. guard cells. Extracellular Ca 2+ modulated the BL‐induced stomatal opening in a dose‐dependent manner, and an application of 5 μM Ca 2+ 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 Ca 2+ , but K + influx and stomatal opening were inhibited by SNP when Ca 2+ was added to the bath solution. Interestingly, although both SNP and BL could activate the plasma membrane Ca 2+ channels and induce the rise of cytosolic Ca 2+ , the change in levels of Ca 2+ channel activity and cytosolic Ca 2+ concentration were different between SNP and BL treatments. SNP at 100 μM obviously activated the plasma membrane Ca 2+ channels and induced cytosolic Ca 2+ rise by 102.4%. In contrast, a BL pulse (100 μmol/m 2 per s for 30 s) slightly activated the Ca 2+ channels and resulted in a Ca 2+ rise of only 20.8%. Consistently, cytosolic Ca 2+ 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 Ca 2+ 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.