Abscisic acid (ABA)-induced stomatal closure is mediated by a complex, guard cell signalling network involving nitric oxide (NO) as a key intermediate. However, there is a lack of information concerning the role of NO in the ABA-enhanced stomatal closure seen in dehydrated plants. The data herein demonstrate that, while nitrate reductase (NR)1-mediated NO generation is required for the ABA-induced closure of stomata in turgid leaves, it is not required for ABA-enhanced stomatal closure under conditions leading to rapid dehydration. The results also show that NO signalling in the guard cells of turgid leaves requires the ABA-signalling pathway to be both capable of function and active. The alignment of this NO signalling with guard cell Ca(2+)-dependent/independent ABA signalling is discussed. The data also highlight a physiological role for NO signalling in turgid leaves and show that stomatal closure during the light-to-dark transition requires NR1-mediated NO generation and signalling.