Thirty percent of infants exposed in utero to SSRIs display behavioral and physiological abnormalities in the first few weeks after birth including increased incidence of pulmonary hypertension. Rats exposed from postnatal day (PN) 1–21 to SSRIs display persistent neurobehavioral abnormalities which include severe deficits in social interactions and expression of serotonergic neurons. Disturbances in serotonin levels result in alterations in mood, sleep, sexuality, and depression. SSRIs have been developed to restore serotonin homeostasis. Adult treatment with SSRIs cause increased water resorption by increasing ADH secretion or increased aquaporin‐2 (AQ‐2) channels in the collecting ducts. The goal of this study was to investigate the lasting effects of early life SSRI exposure on AQ‐2 distribution in the kidneys. Long Evans rats ( 30 male, 30 female) were treated from PN 1–21 with 0.1 mL s.c. of either saline or citalopram (5mg/Kg, 10 mg/Kg, or 20mg/Kg). Animals were sacrificed at PN‐180. Distribution of AQ‐2 and glomeruli size was evaluated. The results show a dose dependent increase in AQ‐2 distribution within the kidney tubules without alterations in glomerular size (p<0.05). No gender differences were observed, which is in contrast to the neurobehavioral effects of early life citalopram exposure. Additional research is needed to determine if ADH secretion or an increase in corticosteroids leads to increased aquaporin‐2 distribution. Supported by RR‐017701 to IAP and KLS and MH‐084194 to RCSL.