Nitric oxide blocks blue light-induced K+ influx by elevating the cytosolic Ca2+ 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.