The effects and the relationship between salicylic acid (SA) and nitric oxide (NO) on Vicia faba L. stomatal movement were studied. The results here showed that exogenous SA and NO induced stomatal closure, 100 μmol/L SA induced a rapid and striking NO increase in the cytosol of guard cells. This phenomenon was largely pre-vented by 200 μmol/L 2-phenyl-4,4,5,5-tetramethylimida-zoline-1-oxyl-3-oxide (PTIO), a specific NO scavenger, and 25 μmol/L NG-nitro-L-Arg-methyl eater (L-NAME), an in-hibitor of NO synthase (NOS) in mammalian cells that also inhibits plant NOS. In addition, SA-induced stomatal closure was largely prevented by PTIO and L-NAME. These results provide evidence that guard cells generate NO in response to SA via NOS-like activity, and that such NO production is required for full stomatal closure in response to SA. H-(1,2,4)-oxadiazole-[4,3-α]quinoxalin-1-one (ODQ), an inhibitor of guanylate cyclase, and nicotinamide, an antago-nist of cADPR production, inhibited the effects of SA- and NO-induced stomatal closure. It suggests that both cGMP and cADPR might mediate the signal transduction of SA and NO-induced stomatal closure.