Loss of control over coping strategies can result in the development of impulsive/compulsive spectrum disorders (ICSDs) such as Obsessive-Compulsive Disorder or trichotillomania. Rats, like humans, show individual differences in their tendency to engage in and maintain control over coping behaviours. While most rats exposed to a schedule-induced polydipsia (SIP) procedure develop a controlled coping response, namely polydipsic drinking, some engage in excessive, compulsive drinking, or hyperdipsia. The development of hyperdipsia, to which highly impulsive rats are particularly vulnerable, depends on noradrenergic mechanisms as it is prevented by the noradrenaline reuptake inhibitor, atomoxetine. However, whether noradrenergic mechanisms also underlie the maintenance of well-established compulsive coping or if other traits confer vulnerability to its development, are unknown. In two longitudinal studies in male Sprague Dawley rats, we investigated whether well-established hyperdipsia is influenced by atomoxetine and if its development is predicted by the ICSD-relevant sign-tracking trait. Sign-tracking predicted faster acquisition of adjunctive drinking but not the transition to hyperdipsia, which goal-tracking protected against. Surprisingly, chronic atomoxetine exacerbated well-established hyperdipsia. Post-mortem qPCR assays revealed that the exacerbation of compulsive coping by atomoxetine was associated with increased mRNA levels of the markers of cellular activity and plasticity c-fos and Zif268 across the dorsal striatum. Atomoxetine also altered the hyperdipsia-specific transcriptomic landscape of the nucleus accumbens shell and the pattern of c-fos and Zif268 expression in the amygdala-accumbens system. These results provide new insights into the biobehavioural basis of compulsive behaviours, revealing a differential noradrenergic control of the development and the expression of compulsive coping