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Human central diabetes insipidus (CDI) is a neurobiological syndrome characterized by the presence of hypotonic polyuria, hypernatremia, and polydipsia. CDI can be acquired (aCDI) as the result of brain damage to magnocellular neurosecretory cells or fibers that constitute the hypothalamic-neurohypophyseal system or can be caused by genetic disorders (hereditary CDI). aCDI can be experimentally induced by various surgical interventions, including neurohypophysectomy, pituitary stalk compression (PSC), hypophysectomy, and hypothalamic mediobasal lesions. CDI has been associated with a deficient production of arginine vasopressin (AVP) (the antidiuretic hormone secreted by magnocellular system), while more recently, aCDI animal studies also suggest the possible involvement of oxytocin (OT) (a natriuretic-promoting hormone secreted by neurosecretory systems) and other factors related to serum fluid concentration. Both humans and animals with aCDI may benefit from the combined administration of AVP and OT and, importantly, from a low-sodium diet. Moreover, increased OT levels are observed in Brattleboro rats (with mutated AVP gene), which may explain the regulatory hydromineral capacity shown by these animals after hydromineral challenges. In short, the symptoms shown by the different CDI animal models suggest the involvement of additional factors besides the absence of AVP, which appear to depend on the particular neurobiological systems affected in each case.

Animal Models of Central Diabetes Insipidus: Oxytocin and Low-Sodium Diets as Complementary Treatments