Calcium is an important component in the signal transduction pathway(s) by which stomatal guard cells respond to external stimuli. Increases in guard cell cytosolic free calcium ([Ca2+]cyt) have been demonstrated in response to stimuli that cause both stomatal opening (auxins) and closure (abscisic acid (ABA), elevated CO2, oxidative stress and external calcium). Several different signalling intermediates have been identified that are involved in the generation of stimulus-induced increases in guard cell [Ca2+]cyt. The calcium-mobilizing second messenger cyclic ADP-ribose has been shown to be a component of the ABA signalling pathway in guard cells. Blocking cyclic ADP-ribose-mediated calcium release using inhibitors partially abolishes ABA-induced stomatal closure. In addition, phosphoinositide signalling has been implicated in the response of guard cells to ABA. Inhibitors of guard cell phosphoinositide-specific phospholipase C (PI-PLC) partially abolish ABA-induced increases in [Ca2+]cyt and stomatal closure. These data suggest signal redundancy in the response of guard cells to ABA. The paradox that calcium plays an important role in the transduction of signals that result in opposite end responses (i.e. stomatal opening and closure) raises the question: how is specificity encoded in the guard cell calcium signal? Interestingly, stimulus-induced increases in guard cell [Ca2+]cyt exhibit spatial and temporal heterogeneities. For example, ABA and external calcium stimulate characteristic oscillations in [Ca2+]cyt the pattern of which correlates directly with the strength of the stimulus and magnitude of the final response. These oscillations have the potential to increase the amount of information encoded in the changes in guard cell [Ca2+]cyt through the generation of a stimulus-specific calcium signature.