The phenolic hormone salicylic acid (SA) induces stomatal closure. It has been suggested that SA signaling is integrated with abscisic acid (ABA) signaling in guard cells, but the integration mechanism remains unclear. The Ca2+-independent protein kinase Open Stomata1 (OST1) and Ca2+-dependent protein kinases (CPKs) are key for ABA-induced activation of the slow-type anion channel SLAC1 and stomatal closure. Here, we show that SA-induced stomatal closure and SA activation of slow-type anion channel are impaired in the CPK disruption mutant cpk3-2 cpk6-1 but not in the OST1 disruption mutant ost1-3. We also found that the key phosphorylation sites of SLAC1 in ABA signaling, serine-59 and serine-120, also are important for SA signaling. Chemiluminescence-based detection of superoxide anion revealed that SA did not require CPK3 and CPK6 for the induction of reactive oxygen species production. Taken together, our results suggest that SA activates peroxidase-mediated reactive oxygen species signal that is integrated into Ca2+/CPK-dependent ABA signaling branch but not the OST1-dependent signaling branch in Arabidopsis (Arabidopsis thaliana) guard cells.