Body sodium (Na) levels must be maintained within a narrow range for the correct functioning of the organism (Na homeostasis). Na disorders include not only elevated levels of this solute (hypernatremia), as in diabetes insipidus, but also reduced levels (hyponatremia), as in cerebral salt wasting syndrome. The balance in body Na levels therefore requires a delicate equilibrium to be maintained between the ingestion and excretion of Na. Salt (NaCl) intake is processed by receptors in the tongue and digestive system, which transmit the information to the nucleus of the solitary tract via a neural pathway (chorda tympani/vagus nerves) and to circumventricular organs, including the subfornical organ and area postrema, via a humoral pathway (blood/cerebrospinal fluid). Circuits are formed that stimulate or inhibit homeostatic Na intake involving participation of the parabrachial nucleus, pre-locus coeruleus, medial tuberomammillary nuclei, median eminence, paraventricular and supraoptic nuclei, and other structures with reward properties such as the bed nucleus of the stria terminalis, central amygdala, and ventral tegmental area. Finally, the kidney uses neural signals (e.g., renal sympathetic nerves) and vascular (e.g., renal perfusion pressure) and humoral (e.g., renin–angiotensin–aldosterone system, cardiac natriuretic peptides, antidiuretic hormone, and oxytocin) factors to promote Na excretion or retention and thereby maintain extracellular fluid volume. All these intake and excretion processes are modulated by chemical messengers, many of which (e.g., aldosterone, angiotensin II, and oxytocin) have effects that are coordinated at peripheral and central level to ensure Na homeostasis.

Lesions in the hypothalamic median eminence (ME) induce polydipsia and polyuria in male rats. A first experiment was designed to examine the effect of salt consumption (standard 0.25 percent Na+ vs. low-salt 0.04 percent Na+ diet) on the fluid-electrolytic balance (plasma sodium, urinary sodium excretion, urine osmolality) and water intake of ME polydipsic animals. In the first 6 h post-surgery, the natriuretic response was higher in ME-lesioned animals than in control groups. At 24 h post-surgery, however, less sodium was excreted by ME rats fed with a standard salt diet (ME/SS), despite showing no decrease in salt intake, and they evidenced an increase in plasma sodium concentration and water intake. Urine osmolality was significantly higher in control animals than in either ME-lesioned group. In experiment 2, hypertonic NaCl administration (2 ml/2M) increased the polydipsic behavior of ME-lesioned but not control rats (day 2). Animals deprived of food/salt showed a significant reduction (on day 2) in the initial (day 1) polydipsia, which increased on day 3 when the animals had access to a standard-salt diet. These results suggest that the reduced natriuretic response and the consequent sodium retention observed in ME animals may exacerbate the hydromineral imbalance of this polydipsic syndrome.

Enteral nutrition is often mandatory, especially for patients in vegetative or minimally conscious state. However, its application is nonviable in certain cases due to various adverse effects. Some of these are explained by absence of the cephalic phase of digestion, during which exocrine, endocrine, and motor physiological responses prepare the digestive system to receive, digest, transform, and utilize ingested nutrients. These responses result from the stimulation by nutrients of cephalic sensory systems, mainly in the oropharyngeal cavity, and can also be elicited by food-related thoughts or expectations. The digestive system appears able to rapidly assess the suitability of food and transmit this information to the brain. The vagus nerve and its brainstem relays in the caudal nucleus of the solitary tract (NST) and parabrachial complex appear to participate in the anatomic pathway responsible for this rapid processing. Thus, blockade of the vagus nerve, NST, or external lateral parabrachial region (LPBe) interrupts expression of conditioned taste preferences induced by administration of “predigested” food, while LPBe activation by electric stimulation generates similar preferences to those observed after cephalic food administration. This review may help design enteral diets better adapted to digestive physiology and develop pharmacological interventions against adverse effects of enteral nutrition.

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.